While androgen receptor (AR) signaling is considered the most critical pathway in hormone-sensitive disease, hormone-refractory tumors, which emerge after failing hormone deprivation therapy, are governed by the activation of other tumor-promoting networks, such as the phosphatase and tensin homolog (PTEN) loss of function-associated activation of the protein kinase B/mammalian target of rapamycin (AKT/mTOR) cell survival signaling pathway [2,3,4,5,6,7]. The gene discussed is AKT1; the disease is neoplasm.