Collectively, tumor heterogeneity, clonal evolution, and lineage plasticity underscore the complexity of prostate cancer, as historical multiregion studies have dismantled the simplistic notion of a single-driver event, and single-cell analyses have reinforced that evolving subclones exploit distinct molecular pathways—from androgen receptor variants to transitions toward treatment-emergent neuroendocrine prostate cancer—to overcome therapeutic barriers [68]. This evidence concerns the gene AR and neoplasm.