To collect evidence that supports this idea, we considered our previous findings that the Alox5 gene plays an essential role in functional regulation of LSCs for both PV and CML [15,16], two different types of myeloproliferative neoplasms driven by JAK2V617F and BCR-ABL, respectively. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.