Moreover, in castration-resistant prostate cancer, CPT1B plays a role in promoting cancer, and the androgen receptor (AR) has a direct binding target in its promoter region, which can directly inhibit its expression by transcription, while the increased expression level of CPT1B can promote the castration resistance of prostate cancer cells, as well as proliferation and migration, by activating AKT phosphorylation [92]. This evidence concerns the gene AR and Familial prostate cancer.