Taken together, these data suggest that Her2 is signalling through Raf and ultimately through c-Jun (AP-1), as we have suggested previously (Edwards et al, 2004), to circumvent AR activity after the tumour has become insensitive to androgens, as AP-1 has been shown to act independently of AR to activate some of the AR-associated genes (Sato et al, 1997). The gene discussed is JUN; the disease is neoplasm.