This hypothesis is supported by a study on BCR::ABL1 p. T315I-positive CML in mice demonstrating that the presence of the p. T315I mutation affected cell adhesion and deposition of FN1 thereby enhancing malignant progression, while the administration of FN1 or an integrin-like kinase inhibitor to enhance FN1 expression increased the overall survival of CML cells (Kumar et al., 2020). This evidence concerns the gene FN1 and chronic myelogenous leukemia, BCR-ABL1 positive.