This is because: i) they occupy strategic locations at the host—pathogen interface; ii) they quickly amass at infection sites where they respond to a variety of bacteria and fungi [20–22]; iii) they exhibit an effector memory-like phenotype [11] and are capable of producing pro- and/or anti-inflammatory cytokines (e.g., IFN-γ, TNF-α, IL-4, IL-10) readily, amply and promptly after iTCR stimulation. This evidence concerns the gene IFNG and infection.