The most significant trait of CML LSC is BCR-ABL1 independence, which makes them autonomous from the fusion protein TK for proliferation and survival and drives their resistance to TK inhibitors IM, Nilotinib and Dasatinib, hence providing a sanctuary for the disease relapse upon drug withdrawal and a putative source of drug-resistance [5]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.