While elegant studies by different groups have demonstrated that negative reciprocal feedback between PI3K and AR signaling pathways can act as an AR-independent mechanism to develop CRPC in PTEN-deficient models of PCa [40,43], there is evidence to suggest a functional interplay between the PI3K/AKT pathways and AR, wherein AR and AKT work synergistically to promote PCa initiation and progression [44]. The gene discussed is AKT1; the disease is posterior cortical atrophy.