Since excess levels of EGF and EGFR are produced by both PCa cells and tumor-specific stromal/fibroblasts, it is likely that EGFR signalling in cancer cells is activated via the production of binding ligands by both cancer cells and tumor-specific stromal/fibroblasts through paracrine and autocrine loops, leading to the growth and survival of PCa cells in the absence of androgens (Di Lorenzo et al. 2002; Traish and Wotiz 1987). The gene discussed is EGF; the disease is posterior cortical atrophy.