In support of this hypothesis, we previously identified that the downregulation of Rab interactor 1 (RIN1) and Bridging integrator 1 (BIN1), two proteins directly involved with Rab-mediated receptor tyrosine kinase intracellular trafficking, caused aberrant and constitutive receptor signaling and are often observed deregulated in CML-resistant patients [30]. The gene discussed is BIN1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.