To identify positive regulators of the response, following the first round of screening, we retained clones that reduced the infection-induced expression of nlp-29p::gfp by 20 % or more in both of the tests (i.e., provoked a Nipi phenotype), but excluded those that altered the expression of the control col-12p::dsRed transgene or reduced the average size of the worms more than when we knocked-down the known signaling component rack-1 [9]. This evidence concerns the gene RACK1 and infection.