Further, in vitro functional studies revealed that HMGCS2 was up-regulated in HG-induced cardiomyocytes, and silence of HMGCS2 could promote cell viability, inhibit apoptosis, inflammation, and oxidative stress, which subsequently attenuated HG-induced DCM in cardiomyocytes. The gene discussed is HMGCS2; the disease is familial dilated cardiomyopathy.