For instance, IL-6, commonly expressed at high circulating levels in patients with different cancers, increases AR activity in a ligand-independent manner via the protein kinase A (PKA), PKC and MAPK pathways (18, 19) Similarly, an enhanced AR activation and nuclear localization is induced by epidermal growth factor (EGF) and insulin-like growth factor (IGF) and leads to the activation of MAPK signaling (22) (Figure 2). This evidence concerns the gene EGF and cancer.