Large-scale sequencing studies have demonstrated recurrent disruptions in androgen receptor (AR) signaling, DNA damage repair (DDR) pathways, PI3K/AKT signaling, and frequent loss of critical tumor suppressors such as TP53, PTEN, and RB1, underscoring the multiplicity of prognostic and potentially actionable molecular events in this malignancy [2,3]. The gene discussed is AR; the disease is neoplasm.