NLRP3-knockout mice with keratitis induced by HSV1 developed more severe disease than infected wild-type animals, with stromal keratitis lesions occurring earlier and having more angiogenesis; this result may be related to the nuclear translocation of the NLRP3-IRF4 complex in Th2 cells, which promotes the expression of the IL-4, IL-5, and IL-13 genes to fight the HSV1 infection [80, 81]. The gene discussed is NLRP3; the disease is keratitis.