While structure-function analysis, shRNA-mediated knockdown, genetic knockout, and pharmacological inhibition experiments clearly indicate an essential role of Prmt1 in MOZ-TIF2 leukemia, it remains to be determined whether Prmt1 recruitment per se is sufficient and the sole function of the N-terminal minimal transformation domain required for MOZ-TIF2-mediated leukemogenesis. This evidence concerns the gene PRMT1 and leukemia.