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. Here, MYC is linked to myocardial infarction.