The effect of AKT on CTNNB1 phosphorylation could be either direct phosphorylation35 or indirectly regulation via the GSK3β, resulting in the accumulation of CTNNB1.36 This interaction between CTNNB1 and AKT conferred resistance to AKT inhibitor in colon cancer.37 This could explain the higher IC50s of AKT inhibitor AZD5363 in MPNST cancer cell lines (Figure S5). The gene discussed is AKT1; the disease is colonic neoplasm.