Our findings are consistent with previous studies demonstrating the anti-apoptotic effects of EA, which was shown to ameliorate apoptosis in pancreatic beta cells in type 2 diabetes [69], in a busulfan-induced rat model of testicular damage [70], and in amikacin-induced nephrotoxicity [71] by downregulating Bax and upregulating Bcl expression. The gene discussed is BAX; the disease is type 2 diabetes mellitus.