Interestingly, the three genes most highly upregulated upon infection in wild-type brains (Ankrd34c, Cbln4, and Kdm4d), as well as several downregulated genes (Col7a1, Col16a1, and Lama5) may influence remodeling of or are themselves extracellular matrix proteins, suggesting that long-lasting effects of T. gondii infection, even in the absence of persistent cysts, may arise either through continued remodeling of the extracellular matrix (ECM) to recover and rebuild after infection, or due to continued circulating T. gondii antibodies (52, –, 54). The gene discussed is KDM4D; the disease is infection.