They insisted that (1) RB loss of function was overrepresented in CRPC and metastatic prostate cancer; (2) RB1 gene loss was frequently observed in CRPC; (3) RB depletion was sufficient to induce castration-resistant tumor growth through AR deregulation; (4) RB depletion resulted in AR mRNA deregulation and protein accumulation through stringent E2F1-mediated regulation; (5) perturbation of the RB/E2F/AR axis was frequently observed in CRPC, resulting in AR upregulation [55]. Here, RB1 is linked to neoplasm.