Finally, impaired glucose metabolism (122) and hyperglycemia are known features of inflammaging, and introduction of Tet2 mutations into hyperglycemic Ins2Akita/+ mice triggered age-dependent increases in mortality, hyperactive inflammation, and progression to an MPN/AML phenotype (68), demonstrating key links between inflammation and aging-associated metabolic phenotypes that may promote CHIP. This evidence concerns the gene STUB1 and myeloproliferative disorder.