To determine whether Akt inactivation mediates the anti-cervical cancer effects of GJB5 silencing, we introduced a constitutively-active Akt1 (caAkt1, S473D) mutant into GJB5-silenced priCC-1 cells, and it completely restored Akt-S6K1 phosphorylation without affecting GJB5 protein expression (Fig. 8D). The gene discussed is AKT1; the disease is cervical cancer.