In light of these analyses from both primary and secondary dengue, we posit that DENV-elicited inflammation may further reduce the likelihood of IgA-mediated ADE—but may increase the likelihood of IgG-mediated ADE due to the suppressed expression of FcaR and increased expression of FcγRs relative to monocytes at homeostasis. The gene discussed is FCAR; the disease is dengue disease.