Although the growth of LNCaP/IL-6#1 was significantly inhibited compared with that of LNCaP/Co under an androgen-deprived condition, Akt and MAPK pathways in LNCaP/IL-6#1, which are generally regarded as a positive regulator of prostate cancer cell growth through the transactivation of AR (Ueda et al, 2002b; Corcoran and Costello, 2003; Lee et al, 2003), appeared to be markedly activated following androgen withdrawal compared with those in LNCaP/Co. Here, IL6 is linked to prostate cancer.