Literature suggests that stimulating SRC with MCB-613 (and its derivatives) may be a potential therapeutic method to inhibit cardiac dysfunction after MI.[36] Literature suggests that stimulating SRC with MCB-613 (and its derivatives) is a potential therapeutic approach to inhibit cardiac dysfunction after MI.[37] c-Myc maintains PI3K/Akt signaling activation by forming a positive feedback loop with lncRNA small nucleolar RNA host gene 1, thereby inducing cardiomyocyte proliferation and improving cardiac function after MI. This evidence concerns the gene AKT1 and myocardial infarction.