In this review, we aim to summarise our current understanding of how AAM is dysregulated in PCa in comparison to physiological conditions, especially focusing on key altered genes, amino acid residues (glutamine, tryptophan, leucine, arginine, methionine, histidine, serine and glycine) and amino acid signalling pathways (mTOR and GCN2). This evidence concerns the gene MTOR and posterior cortical atrophy.