In CML, Bcr-Abl can transcriptionally drive the expression of SNAI2 and post-transcriptionally stabilize SNAI2 protein, and SNAI2 mediates Bcr-Abl-T315I-driven resistance of leukemic progenitor to imatinib mesylate through the repression of pro-apoptotic Puma [21]. Here, SNAI2 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.