In CML, A-to-I editing within the introns of glycogen synthase kinase 3β (GSK-3β) by ADAR1 caused the mis-splicing of GSK-3β with reduced capacity to inactivate β-catenin, thereby facilitating LSCs self-renewal via the activation of β-catenin signaling (Abrahamsson et al., 2009; Jiang et al., 2013). The gene discussed is ADAR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.