Given that Bak is a well-established transcriptional target of p53 56, 57, and that p53 has been involved in regulating mPTP opening across various pathological contexts including cardiac ischemia/reperfusion (I/R) injury and oxidative stress in H9c2 cells 48, NaF-induced neurotoxicity and PC12 cell apoptosis 58, as well as T-2 toxin-induced cartilage degeneration in Kashin-Beck disease models and ATDC5 cell apoptosis 59, we explored whether p53-Bak axis contribute to stress-induced cardiomyocyte necrosis. The gene discussed is BAK1; the disease is Kashin-Beck disease.