ABI1-deficient K562 cells, which express CML fusion protein breakpoint cluster region (BCR)-ABL, show an integrin signaling-mediated quiescence phenotype characterized by increased integrin ⍺4 expression, resistance to BCR-ABL inhibitor imatinib, decreased proliferation, and increased adhesion associated with elevated p130Cas-CRK activation [41]. This evidence concerns the gene ABI1 and chronic myelogenous leukemia, BCR-ABL1 positive.