Additionally, leptin-driven adiposity in mouse models of obesity promotes STAT3-facilitated FAO in intra-tumoral CD8+ T cells at the expense of glycolytic capability [28]; although this FAO shift is crucial for the formation of memory CD8+ T cells [29], the activation process is already compromised by diminished glycolysis, resulting in redundancy as FAO cannot sustain the energetic needs required for effector functions. Here, CD8A is linked to obesity due to melanocortin 4 receptor deficiency.