Taken together, our cellular and organismal studies of Cobll1/PACSIN2/SH3BP1 and clinical analysis of patient samples showed that the Cobll1/SH3BP1/PACSIN2 axis that modulates Rac1 activity regulates drug resistance and disease progression in CML. This evidence concerns the gene SH3BP1 and chronic myelogenous leukemia, BCR-ABL1 positive.