While the Sca1-ETV6-RUNX1 model might have a different reliance on Myd88 signaling or on the cell intrinsic developmental stage where molecular alterations should take place, these results highlight the need to identify downstream mechanisms to provide possible explanations for the inability of Abx-treatment to drive leukemia progression in the Sca1-ETV6-RUNX1 model. This evidence concerns the gene RUNX1 and leukemia.