However, researchers also found that specific silencing of c-FLIPL can effectively inhibit HCT116 tumor growth and induce apoptosis as silencing both splice forms, and c-FLIPL overexpression can dramatically inhibit the growth-inhibitory effects of chemotherapy in vivo setting, suggesting that the c-FLIPL may be the more important regulator of CRC (195). The gene discussed is CFLAR; the disease is neoplasm.