GSEA of these MYR1-dependent effects (Fig. 3C) revealed an apparent contradiction in that one predominant GSEA gene set, “TNF-α signaling via NF-κB,” was the most strongly overrepresented in the set of genes upregulated in both infections (RHΔmyr1 and RH-WT) compared to mock infected, suggesting MYR1 independence (Fig. 2A), and yet the same gene set was also significantly different in the head-to-head comparison, suggesting some dependence on MYR1. The gene discussed is NFKB1; the disease is infection.