For example, IGF signaling has been implicated in the progression from androgen-dependent to androgen-independent states [2], but also has been shown to suppress AR trans-activation via FoxO1 and thus have inhibitory effects on the growth of prostate cancer cells [3], EGF was reported to mimic effects of androgen on the gene expression and independently stimulate growth of androgen-dependent prostate cancer cells [4]. This evidence concerns the gene AR and Familial prostate cancer.