Taken together, current results including preliminary evidence of clinical associations between elevated CAMKK1 and complications due to diabetes, show how blood glucose control may be described as shifting from pro‐homeostatic mechanisms (i.e., satiety and hunger, leptin and ghrelin) to inflammatory control (i.e., TNFα) in T2DM. The gene discussed is CAMKK1; the disease is type 2 diabetes mellitus.