Moreover, we have demonstrated that both GPR107-silencing and NST treatment altered key pathophysiological parameters in PCa in vitro, including a reduction of cell proliferation and migration and modulation of the expression levels of relevant molecular markers (e.g., MKI67, SST5TMD4, AR-v7, etc.), possibly through the modulation of the key AKT pathway. Here, AKT1 is linked to posterior cortical atrophy.