In CML, Bcr-Abl causes constitutive repression of FoxO3a by continued activation of Akt, leading to another mechanism of Bcr-Abl-mediated apoptotic resistance (Khorashad et al., 2008; Scheller et al., 2013). The gene discussed is AKT1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.