A plausible explanation for the development of CML-like disease in Icsbp−/− mice is that when Icsbp is removed, LSK cells could not undergo the transition to apoptotic LSK− cells, and the LSK population could only be regulated through differentiating to become more mature myeloid cells, eventually leading to the development of CML-like disease, as observed in Icsbp−/− mice [19]. This evidence concerns the gene IRF8 and chronic myelogenous leukemia, BCR-ABL1 positive.