GSK3B and schizophrenia: In the case of schizophrenia, targeting GSK3β to indirectly enhance CTNNB1 activities as a transcriptional co-activator could be a possible therapeutic avenue for correcting any impaired gene expression critical to re/myelination, as described in our previous studies [109,111,115], given that GSK3β inhibitors are clinically used in other psychiatric and neurological conditions [116,117,118].