The findings in mouse CML leukemia model and human CML patients indicate that CaMKIIg could be a critical regulator in the progression of CML blast crisis, and they reveal a novel mechanism by which CaMKIIg promotes leukemia stem cell (LSC) self-renewal by inhibiting nuclear p27Kip1 and reawakening dormant LSCs [34,38]. The gene discussed is CDKN1B; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.