Beyond canonical RASGEF function in KRAS‐mutant tumors, SOS1 exhibits unique pathology in BCR–ABL+ leukemia: PH domain‐mediated interaction with BCR–ABL fusion protein confers constitutive kinase activity, enhancing both RASGEF function and RAC1 activation via C‐terminal proline‐rich regions, promoting leukemic cell proliferation [199]. This evidence concerns the gene RAC1 and leukemia.