Our previous work on Gab2 mediated TKI resistance in CML cells suggested that this docking protein, due to its position downstream of both growth factor receptors and Bcr-Abl [7], protects against TKIs as it can be tyrosine phosphorylated by the former and thereby drive the activation of pro-leukemogenic pathways in the absence of Bcr-Abl activity. The gene discussed is GAB2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.