These data imply that, unlike Lgr4/Gpr48, Gdpd3 contributes to the maintenance of CML stemness via effects on multiple pathways, such as by suppressing AKT/mTORC1 signalling, decreasing the expression of GPCR genes, and regulating the interaction between Foxo3a and β-catenin (Fig. 8c). The gene discussed is AKT1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.