These mutations, along with epigenetic reprogramming, facilitate the BCR-ABL1 independent activation of PI3K, MAPK, JAK/STAT, and SRC signaling pathways in CML cells, all of which have been implicated in BCR-ABL1 independent mechanisms of resistance [22]. Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.