In this study, by employing the same inducible NANOG transgene expression system in LNCaP cells that express little endogenous NANOG mRNA [9] and through integrative ChIP-Seq and RNA-Seq analysis combined with biological assays, we discover detailed mechanisms underlying NANOG-mediated somatic cancer cell reprogramming to the therapy-resistant and CSC state, most of which impinge on AR/FOXA1 signaling (Figure 7e). The gene discussed is FOXA1; the disease is cancer.