ABL1 and breast cancer: To gain further insight into how miR-142 deficit drives a BC-like transformation and identify pathways and targets mediating the disease transformation, we performed bulk RNA-seq on LSKs harvested from normal miR-142+/+ (wt) and miR-142−/− (miR-142 KO) mice as well as from leukemic miR-142+/+BCR-ABL (CP CML) and miR-142−/−BCR-ABL (BC CML) mice, two weeks after BCR-ABL induction (Fig. 3a).