Taken together, these findings, as previously mentioned, suggest that CAMKK1's role may shift from pro‐homeostatic mechanisms (i.e., promoting ghrelin‐mediated food intake on one hand and promoting leptin‐mediated satiety on the other) to inflammatory control (i.e., TNFα‐mediated metabolic dysregulation) in patients with T2DM. The gene discussed is LEP; the disease is type 2 diabetes mellitus.