There is considerable evidence to show crosstalk between AR and NFκB (De Bosscher et al. 2006); thus, it is reasonable to postulate that the persistent repression of AR signaling induced by vinclozolin results in androgenic activity that is insufficient to suppress NFκB signaling pathways, resulting in inappropriate activation of NFκB and the emergence of prostatitis. The gene discussed is NFKB1; the disease is prostatitis.