From these results, we concluded that the lack of crp2-1 expression in the mutant larvae does not result from the general defect in the inflammatory response, and the increase in the expression of il1b, il6, and tnfa in the mutant larvae may be due to a compensatory response to the hampered crp2-1 expression, or due to more severe infection and higher bacterial burden in mutant94 larvae compared to AB larvae. The gene discussed is TNF; the disease is infection.