In diabetes, accumulation of advanced glycation end (AGEs) products contributes greatly to excessive production of reactive oxygen species (ROS) (Tang et al., 2019), subsequently inducing inflammation, interrupting cellular homeostasis, upregulating RhoA/ROCK pathway and damaging the corpus cavernosum smooth muscle function to a large extent (Kamenov, 2015; Wang et al., 2016), and all of these largely contribute to the pathogenesis of DMED. The gene discussed is RHOA; the disease is diabetes mellitus.