However, knock-in mice expressing Cbfb-MYH11 with a HABD deletion unexpectedly potentiated its leukemogenic activity, developed leukemia faster, even though hematopoietic defects associated with Runx1-inhibition were partially rescued, suggesting that AML1-dominant inhibition may not be a critical step for leukemogenesis by CBFβ-SMMHC [55]. This evidence concerns the gene CBFB and leukemia.