Progenitor cells of CML patients (CD34+CD38+, CD34+CD38−, CD34+CD38−CD90+) actively evade host immune surveillance through cytokine-mediated downregulation of MHC-II and its master regulator class II transactivator (CIITA), a transcription factor that functions as a molecular switch for MHC-II gene regulation, and may explain why CML stem cells persist despite lifelong TKI treatment (97). The gene discussed is CIITA; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.