In vitro, β-catenin signaling activation via GSK3B was targeting by LiCl2 and MYC-MAX interaction was inhibited by 10058-F4 in order to confirm the cooperation of TCF7L2 and MYC to drive an embryonic program in the blast crisis of CML, especially by regulating some genes that were found to overlap PLURINET and ESCcore signatures: PRMT1, RUVBL1, and WDR77. The gene discussed is MAX; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.