Figure 8 shows our proposed hypothesis for the mechanism of PHB:AR interaction. This report also strengthens the evidence that AR may function as a replication licensing protein in prostate cancer cells as postulated by D’Antonio et al.42 and reviewed in Balk and Knudsen,43 especially given the androgen-mediated E2F1 charge shift (see Supplementary Figure 7B). The gene discussed is AR; the disease is prostate carcinoma.