Taken together, bFGF released ectopically as a result of endothelial damage and pro-inflammatory cytokines upregulated (in part) as a result of hyperglycemia and/or obesity in type 2 diabetes may facilitate (through as yet poorly-defined mechanisms) immune interactions favoring a transition from strongly inhibitory (AECA ≤80%) to less inhibitory or stimulatory AECA having cell-mediated survival >80% in subsets of advancing diabetic CKD. Here, FGF2 is linked to obesity due to melanocortin 4 receptor deficiency.