These alterations include AR gene mutation and amplification (50), and induction of bypass pathways in AR signaling, which include intracrine androgen biosynthesis in PCa, expression of constitutively active, ligand-independent AR splice variants, and non-canonical activation of AR by receptor tyrosine kinases (RTK) in the absence of ligand (51). Here, NTRK1 is linked to posterior cortical atrophy.