It has been suggested that Atoh1 mRNA transcription was facilitated by JNK in normal intestinal epithelium [35], whereas Atoh1 expression was mainly regulated via post-translational modification in CRC development and the activation of AKT could induce the inactivation of GSK3β, which was involved in the ubiquitin-proteasomal degradation of Atoh1 in CRC cells [23,28]. Here, GSK3B is linked to colorectal carcinoma.