To test if secondary genomic “hits” (i.e., gene mutations) cooperated with miR-142 deficit in inducing BC transformation, we subjected BM LSKs harvested from miR-142−/−BCR-ABL at the time of first appearance of circulating blasts (3–4 weeks after BCR-ABL induction) and those from miR-142+/+BCR-ABL mice, to whole genome sequencing. The gene discussed is ABL1; the disease is breast cancer.