Our recent work has proven the hyper-activation of PLK1 serine/threonine kinase and FOXM1 transcription factor in the putative stem cell compartment of CML, identified by CD34+ phenotype, and their role in BCR-ABL1+ LSC persistence under TK inhibitor therapy [8]. The gene discussed is FOXM1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.