The IFN-γ-mediated immune response against T. gondii involves a sophisticated regulatory network centered on three key molecular pathways: (1) The NF-κB pathway, where p65 (RelA) prevents parasite-induced apoptosis and is essential for infection control, as demonstrated by the susceptibility of p65 KO cells; (2) The IRF8-dependent pathway, which orchestrates IL-12 production through TLR11/MyD88 signaling and is critical for dendritic cell function; and (3) The T-bet axis, which directs Th1 differentiation and innate IFN-γ production that feeds back to sustain IRF8 activation [42,43,44]. Here, NFKB1 is linked to infection.