Moreover, the study, including both in vitro and in vivo methods, showed that the inhibition of the BCR-ABL–PI3K–AKT pathway promoted the degradation of β-catenin and reduced the transcription of β-catenin target genes, consequently reducing the tumor-initiating ability of CML cells in xenograft mice [56]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.