AR and neoplasm: The AR‐V7 androgen receptor splice variant is currently the most well‐defined resistance variant, lacking the androgen‐binding domain but retaining an activation domain that promotes tumor growth.[8, 9] In light of this, scholars are striving to identify new therapeutic targets and develop more effective drugs to eradicate CRPC, such as AR‐V7 degraders and the AKT inhibitor Ipatasertib.[10, 11] Nevertheless, the efficacy of these new treatments remains to be definitively established, and resolving Abiraterone resistance in CRPC patients is an urgent priority.