Specifically, in LCL patients, a unique subtype of ILC1 that requires T-bet for differentiation can produce significant amounts of IFN-γ and TNF-α when exposed to cytokines from infected cells, resulting in a more robust Th1 response and consequent classical macrophage activation, as previously observed in inflammatory bowel disease (IBD) and infection-induced colitis [76,77]. Here, IFNG is linked to inflammatory bowel disease.