In our study, AKT‐mediated phosphorylation (T447/S451/S455) emerged as a key regulator of ACLY nuclear translocation, aligns with somatic systems after DNA damage or obesity‐related factors (estradiol, insulin and leptin).[45, 94, 95, 96] Phosphorylated ACLY recruits HAT1 and P300 through direct physical interactions, forming nuclear metabolons that sustain H3K27ac at pluripotency loci (such as Pou5f1). This evidence concerns the gene ACLY and obesity due to melanocortin 4 receptor deficiency.