A broader, analysis of the highly modulated KEGG pathways in a type I context of infection revealed that a substantial number of both pro- (e.g., IL-1a and TNF) and anti-inflammatory (e.g., IL-10) cytokines, chemokines and their relative receptors (e.g., CXCL1, CXCL10) were significantly differentially-regulated upon Δasp5 parasite infection compared to parental lines (Fig 6D, left panel). The gene discussed is TNF; the disease is parasitic infectious disease.