In addition, caspase-8, which was shown to be the main regulator of apoptosis induced by HS16, was activated independent of TRIF in response to HS alone (Supplementary Fig. 5D), while caspase-8 activation was dependent on TRIF in response to LPS plus HS (Supplementary Fig. 5B), suggesting that the mechanisms of cell death induced by HS differs with or without infection. The gene discussed is CASP8; the disease is infection.