In the early hematopoiesis stage, GFI1B acts as an oncosuppressor by driving differentiation toward specific hematopoietic lineages, and reduced GFI1B expression in concert with other signaling cascades blocks the differentiation and upregulates OXPHOS and FAO, which in turn promote LSCs augmentation and lead to an inferior prognosis and chemoresistance in AML patients. This evidence concerns the gene GFI1B and acute myeloid leukemia.