The involvement of ILK in the pathophysiology of BCR-ABL1T315I+ (and BCR-ABL1+) CML, given its linkage to the cytoplasmic domains of integrin β1 and β3, its support of scaffolding proteins [40] and its known role in the deposition of fibronectin by epithelial cells [47]—though opposite from our results in hematopoietic cells—and other ECM proteins [48] was not surprising and may be context dependent. The gene discussed is ILK; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.