TKIs, the front-line treatment of CML, inhibit the oncogenic BCR-ABL tyrosine kinase activity and this induces autophagic flux (Bellodi et al., 2009; Helgason et al., 2013; Baquero et al., 2018). The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.