APC and chronic myelogenous leukemia, BCR-ABL1 positive: The activation of β-catenin in CML is driven by post-translational modifications, namely the BCR-ABL1-mediated phosphorylation at specific tyrosine residues (Y86 and Y654), which enhances protein stability by impairing its recruitment to the adenomatous polyposis coli (APC)/Axin/glycogen synthase kinase-3β (GSK-3β) destruction complex [9].