Establishing a diagnosis of hypersensitivity pneumonitis (HP) and distinguishing it from other forms of interstitial lung diseases represents a common challenge in clinical practice. This review summarizes the latest literature and guidelines on HP while integrating some real-life conundrums. Advances in the understanding of the pathobiology of fibrotic HP and other progressive pulmonary fibrosis have changed how we approach the diagnosis and treatment of interstitial lung disease. Classifications now embrace distinguishing two clinical phenotypes nonfibrotic and fibrotic HP because of distinct disease behavior and prognosis implications. International guidelines on HP were recently published and proposed a framework and algorithm to guide the diagnostic process. The diagnosis of HP relies on the integration of multiples domains clinical assessment of exposure, imaging, bronchoalveolar lavage lymphocytosis and histopathological findings. These features are reviewed in multidisciplinary discussion and lead to an estimation of the degree of confidence for HP diagnosis. Further research is warranted to improve knowledge on the pathophysiology of HP and ultimately improve its diagnostic approaches.The diagnosis of HP relies on the integration of multiples domains clinical assessment of exposure, imaging, bronchoalveolar lavage lymphocytosis and histopathological findings. These features are reviewed in multidisciplinary discussion and lead to an estimation of the degree of confidence for HP diagnosis. Further research is warranted to improve knowledge on the pathophysiology of HP and ultimately improve its diagnostic approaches. Epidemiological and clinical observations as well as familial clustering support the existence of a genetic predisposition to sarcoidosis. AGK2 mouse In this article, we review the most recent findings in genetics of sarcoidosis and discuss how the identification of risk alleles may help advancing our understanding of disease etiology and development. Genetic studies of sarcoidosis phenotypes have identified novel and ancestry-specific associations. Gene-environment interaction studies highlighted the importance of integrating genetic information when assessing the relationship between sarcoidosis and environmental exposures. A case-control-family study revealed that the heritability of sarcoidosis is only 49%, suggesting the existence of additional important contributors to disease risk. The application of whole-exome sequencing has identified associations with disease activity and prognosis. Finally, gene expression studies of circulating immune cells have identified shared and unique pathways between sarcoidosis and other granulomatous diseases. Sarcoidosis genetic research has led to the identification of a number of associations with both sarcoidoses per se and disease phenotypes. Newer sequencing technologies are likely to increase the number of genetic variants associated with sarcoidosis. However, studying phenotypically and ethnically homogeneous patient subsets remains critically important regardless of the genetic approach used.Sarcoidosis genetic research has led to the identification of a number of associations with both sarcoidoses per se and disease phenotypes. Newer sequencing technologies are likely to increase the number of genetic variants associated with sarcoidosis. However, studying phenotypically and ethnically homogeneous patient subsets remains critically important regardless of the genetic approach used. Previous studies mainly described a role for organic agents as possible triggers for sarcoidosis. In this review, we address recent studies suggesting a possible role for inorganic elements, such as metals or silica in sarcoidosis pathogenesis. Several epidemiological papers suggest that inorganic agents, either by environmental exposures or occupational activities, could trigger sarcoidosis. Association between inorganics and sarcoidosis is also described in several recently published case reports and studies demonstrating immunological sensitization to inorganic agents in sarcoidosis patients.Studies comparing chronic beryllium disease (CBD) and sarcoidosis suggest that although antigenic triggers may differ, underlying processes may be comparable.Besides the fact that a growing number of studies show a possible role for inorganic triggers, it is also suggested that inorganic triggered sarcoidosis may result in a more severe phenotype, including pulmonary fibrosis. We can use the knowledge already gained on CBD pathogenesis to conduct further research into role of inorganics, such as metals and silica as antigens in sarcoidosis. Given the importance of a lymphocyte proliferation test (LPT) in diagnosing CBD, it seems obvious to also implement this test in the diagnostic work-up of sarcoidosis to identify patients with an inorganic antigenic trigger of their disease.We can use the knowledge already gained on CBD pathogenesis to conduct further research into role of inorganics, such as metals and silica as antigens in sarcoidosis. Given the importance of a lymphocyte proliferation test (LPT) in diagnosing CBD, it seems obvious to also implement this test in the diagnostic work-up of sarcoidosis to identify patients with an inorganic antigenic trigger of their disease. Treatment options for Group 3 pulmonary hypertension, characterized as secondary to chronic hypoxia or lung disease, remain an elusive holy grail for physicians and patients alike. Despite increasing identification and investigation into this pulmonary vasculopathy group with the second-highest frequency and highest mortality, there are no therapeutic interventions that offer the significant improvements in morbidity and mortality comparable to those benefiting other pulmonary hypertension groups including pulmonary arterial hypertension. This review examines the data on available and emerging Group 3 pulmonary hypertension treatments. Pulmonary vasodilators have yielded equivocal results in this patient population, although recent evidence shows modestly improved outcomes with inhaled treprostinil in interstitial lung disease-associated pulmonary hypertension. With pulmonary vasodilators providing limited benefit, emerging data support the right ventricle as a potential treatment target in Group 3 pulmonary hypertension.