Mechanistically, the high-glucose tumor microenvironment caused by diabetes mellitus could provide more acetyl-CoA and upregulate TRIB3 acetylation and protein stability, transforming metabolic signals to oncogenic signals.101 It seems reasonable to speculate that diabetes-associated hyperglycemia and high-glucose diet might promote tumor development by upregulating the protein acetylation described above. This evidence concerns the gene TRIB3 and neoplasm.