,345 Such postulation is strengthened by the findings that (1) METTL3 knockout before mice MI preserves cardiac function and structure afterward,140 and (2) METTL3 promotes cardiomyocyte pyroptosis and myocardial I/R injury in rats via an m6A-dependent DGCR8-mediated pri-miR-143-3p maturation to yield miR-143-3p to finally suppress protein kinase C epsilon type (PRKCE).142. The gene discussed is METTL3; the disease is myocardial infarction.