Implicated in atherosclerosis, hypertension, aortic dissection, cardiac fibrosis, and cardiomyopathy; regulation is time-dependent and can have protective or detrimental effects on the heart depending on duration and kinetics; stimulates cardiomyocyte hypertrophy, promotes apoptosis, and impairs cardiac contractile function; and, activates multiple signaling pathways like NF-κB, PI3K-Akt, MAPK, and JAK-STAT pathways to regulate genes involved in inflammation and immunity and hence a potential target for therapeutic interventions. This evidence concerns the gene SOAT1 and atherosclerosis.