The results of Jiaqi Liu and colleagues showed that exogenous H2S mitigated dysfunction of arterial endothelial cells by decreasing the expression levels of marker proteins including Von Willebrand factor (vWF), Integrin beta-1 (ITGβ1) and GP1β A and reduced apoptosis of rat aortic endothelial cells (RAECs) by decreasing the expression levels of apoptosis-related proteins and mitigating mitochondrial damage in a diabetes model. This evidence concerns the gene ITGB1 and diabetes mellitus.