This mechanism explains the abnormal splicing of GSK3B in CML cells: during CML progression, IFNγ- and BCR-ABL1-stimulation of expression of ADAR1 results in a propensity to change A to I nucleotides, possibly affecting splice donor or acceptor sites [131]. The gene discussed is IFNG; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.