Changes in the balance of GSK3β2/GSK3β1 isoforms due to alternative splicing regulation could have a broad impact in cancer initiation or progression, not only owing to an effect on ER and AR protein level, as reported in this work but also owing to the key role of GS3Kβ in the β-catenin homeostasis and its cross-talk with WNT-signaling pathway. The gene discussed is AR; the disease is cancer.