NFKB1 and infection: NF‐κB activation may suppress apoptosis and enhance cell migration, allowing for cell proliferation for further infection.[26] The TgMIF‐induced pro‐inflammatory response may not only reduce parasite burdens in the host but also cause tissue damage, allowing pathogens to bypass tissue barriers and disseminate to other host tissues, which may explain T. gondii’s symbiotic relationship with humans.