Studies have shown that combined therapy with TKIs and IFN-α produces synergistic effects evidenced by deeper molecular responses and eradication of mutant CML cells [109], and IFN-α monotherapy allows for the discontinuation of imatinib because it maintains the molecular remission levels achieved by prior combined therapy with TKIs and IFN-α [110]. The gene discussed is IFNA2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.