Exemplifying this notion even further is the discovery that AHI-1, a scaffolding protein found to be highly deregulated in CML LSCs, directly interacts with multiple proteins, including BCR-ABL, JAK2, and DNM2, to mediate CML LSC properties and confer TKI resistance [176,177,200]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.