This cytokine milieu drives metabolic inflexibility through (a) peripheral insulin resistance; TNF-α and IL-6 suppress GLUT4 translocation in muscle [24], (b) hepatic steatosis; IL-6 stimulates de novo lipogenesis while impairing lipid oxidation [29], and (c) β-cell dysfunction; chronic IL-1β exposure reduces insulin production capacity [28]. The gene discussed is IL6; the disease is steatosis.