AKT1 and adenocarcinoma: Supporting its role in lineage plasticity, N-Myc overexpression, combined with activated AKT serine/threonine kinase 1 (AKT) or PTEN loss, induces invasive tumors with adenocarcinoma, NEPC, mixed or aberrant phenotypes [95,99] with a prevalence of NEPC after prolonged castration [99].