MERTK and fibrosis: Consistent with this viewpoint, several groups recently did show that increased efferocytosis of apoptotic CMs is able to resolve cardiac inflammation, reduce cardiac fibrosis, increase angiogenesis, and improve cardiac function after myocardial I/R in mice through modification of efferocytotic receptors (i.e., MERTK) (16, 21–23) and other factors (MFEG8, VEGFC, S100A9) (17, 48, 49).