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). The gene discussed is AKT1; the disease is obesity due to melanocortin 4 receptor deficiency.