The increased expression of integrin β3 decelerated CML progression, while knockdown of Integrin-linked kinase (Ilk) led to an increase in fibronectin deposition by T315I mutant cells, with prolonged survival in xenogeneic and syngeneic murine transplantation models [100], offering an additional example of the therapeutic manipulation of the levels of extracellular matrix proteins (e.g., fibronectin) against TKI-resistant CML. The gene discussed is FN1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.