Our data with selonsertib support the concept that reducing ASK1 activity in the heart is a desirable strategy for reducing fibrosis and thus the workload of the heart in disease states such as hypertension and is independent of a direct effect on blood pressure.36 Other studies with genetically modified mice indicate that ASK1 is also a strong therapeutic target in myocardial infarction in which inhibition of ASK1 may facilitate cardiomyocyte survival. The gene discussed is MAP3K5; the disease is Hypertension.