Second, since the expression of the LSC master regulator SPI1 can be reversibly regulated by epigenetic mechanisms (Figures 9–10), this model would predict poorer outcomes if leukemia controlled by such a mechanism was treated with 5-AZ or similar agents and would suggest that the reactivation of SPI1 expression could be a potential mechanism for LSC-mediated therapeutic resistance. The gene discussed is SPI1; the disease is leukemia.