In line with this, our study revealed that both SOS1 degradation by SIAIS562055 and SOS knockdown by siRNAs enhanced the intracellular content of imatinib along with the enhanced expression of SLC22A4 in BCR–ABL+ CML cells, indicating that downregulation of SOS1 has the potential to enhance the efficacy of imatinib in cases where TKI resistance is not solely linked to the BCR–ABL fusion gene. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.