Upon overnutrition, ATMs have been reported to switch from type 2 (M2; CD11c−CD206+) to type 1 (M1; CD11c+CD206−) polarization states, promoting local and systemic inflammation and insulin resistance.[3, 6, 7] However, the identification of balanced M0 (CD206−CD11c−)[8] and mixed (CD206+CD11c+)[9] phenotypes indicates the existence of additional subtype diversity.[10, 11] Targeting of maladaptive adipose tissue macrophage (ATM) phenotypes has the potential to restore the function of ATMs for the homeostasis of adipose tissue in obese individuals. This evidence concerns the gene ITGAX and overnutrition.