Here, we demonstrate a requisite role for JAK1 activity in cardiomyocyte sensing and responding to OSM that is predominantly released into the circulation by immune cells [74], which has implications for intercellular communication and cardiac adaptation not only to myocardial infarction and heart failure but also the cardiac response to a myriad of chronic diseases and other conditions associated with inflammation. The gene discussed is JAK1; the disease is myocardial infarction.