Hyperglycemia was suggested to foster DN-associated RCC development [89] by (i) hyperactivating glycolysis (reported in transcriptomic/metabolomics analysis of diabetic mouse kidneys [90]) and (ii) activating the AKT/mTOR and the insulin growth factor (IGF) proliferative signaling pathways, both shown to be activated in DN in mouse models of diabetes [91,92]. Here, IGF1 is linked to liver dysplastic nodule.