Among the effector genes upregulated by infection with Enterococcus were three genes that had previously been demonstrated to mediate C. elegans resistance to pathogens: sodh-1 (sorbitol dehydrogenase) and cyp-37B1 (cytochrome P450), whose decreased expression caused enhanced susceptibility to killing by S. aureus [1], and ilys-3, an invertebrate lysozyme effector required in the pharynx and in the intestine to prevent the accumulation of bacterial cells in the gut lumen and to protect against M. nematophilum [21]. Here, SORD is linked to infection.