Interestingly, increased β-catenin expression may be a result of aberrant splicing of GSK3B, as demonstrated in a study of CML patients, in which CML cells from four of seven patients in blast crisis and one of four in chronic phase CML showed mis-splicing of GSK3B, yielding a form that did not interact with AXIN and was unable to phosphorylate β-catenin [229]. The gene discussed is AXIN1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.