Thus, BMI1 acts as a major regulator of CSC self-renewal across multiple hematological and solid tumors, including AML, CRC, and brain cancer.163–165 In these malignancies, deregulated BMI1 expression and PRC1 activity enable transcriptional programs that sustain stem-like properties, thereby promoting cancer development and progression. This evidence concerns the gene BMI1 and acute myeloid leukemia.