Consistent with the notion that F4/80+TIM4− ATMs highly express pro-inflammatory genes and contribute to the expansion of the ATM pool in obesity, ultimately promoting diet-associated inflammation, here, GPSM1f/f; Lyz2-Cre mice actually had fewer F4/80+CD11c+ pro-inflammatory M1-like ATMs but more F4/80+CD206+ anti-inflammatory M2-like ATMs, both in the eWAT and scWAT (Fig. 3d, e), confirming a diminished inflammatory environment in GPSM1f/f; Lyz2-Cre mice. The gene discussed is ATM; the disease is obesity due to melanocortin 4 receptor deficiency.