Nevertheless, while the current studies could not rule out the possibility that FL118-mediated inhibition of p-AKT and p-ERK1/2, as well as total AKT and total ERK1/2 by FL118, may play a role in FL118 anticancer efficacy, these signaling pathways may not play the critical determinant role in FL118-mediated inhibition of bladder cancer cell viability and the induction of apoptosis. The gene discussed is MAPK3; the disease is urinary bladder cancer.