Although this suggests a potential role for AKT in mediating the obesity-driven increase in PDA growth3, 28–32, no significant changes in AKT phosphorylation (T308 or S473) were detected in Obese-CFP compared to Lean-CFP tumors (n = 12, Fig. 6c and Supplementary Fig. 9). The gene discussed is AKT1; the disease is obesity due to melanocortin 4 receptor deficiency.