It was also reported that prostate cancer cells expressing the AR variants were resistant to the second-generation antiandrogen MDV3100 [124], whereas another study showed that castration-resistant growth mediated by the AR variants was blocked by MDV3100 or by selective siRNA silencing of full-length AR, indicating that some AR truncated variants require full length AR to drive castration-resistant progression of prostate cancer [116]. Here, AR is linked to prostate cancer.