In addition, taking advantage of preclinical models—deficient in adaptive immune effectors, Rag2−/− mice and ILCs, Rag2−/−IL2−/− mice—it has been shown that the promotion of an M1-like phenotype (CD68+F4/80+) of the monocyte/macrophage population was associated with the expansion of ILC2/3 (i.e., CD117+KLRG+ group ILC2s and CD56+CD117+Nkp46+ group ILC3s) precursors that benefit the control of HFD-induced obesity [16]. This evidence concerns the gene KIT and obesity due to melanocortin 4 receptor deficiency.