When one now considers the history of LNCaP—40 years of culture (since 1978) initially in growth medium containing 15% FCS, selection for a fast growing clone, changes in karyotype (4 X chromosomes in 1979; now, only one AR copy in the FGC clone) a median chromosomal number of 85-89 and an extreme phenotypic plasticity based on culture conditions [70,85,92]—LNCaP does allow the study of AR gene regulation, but is it still the ideal model (in 2020) on which to base studies of the precise molecular mechanisms of prostate cancer AR response and treatment resistance? This evidence concerns the gene AR and Familial prostate cancer.