However, due to a notorious difficulty to investigate rare BCR-ABL-positive residual clones, most of the suggested imatinib and TKI persistence mechanisms have been derived using cell lines or pre-therapeutic CD34+ CML samples, which may not exactly reflect in vivo regulations during long term persistence [8, 85–90]. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.