Guo et al. reported that seven days after corneal infection by HSV-1, tear films and trigeminal ganglia from RIPK3−/− mice and Casp8−/− RIPK3−/− mice exhibited 10-fold higher amounts of infectious virus particles, relative to wild-type animals, suggesting that impairment of necroptosis and/or apoptosis enhances viral spread [82]. This evidence concerns the gene RIPK3 and corneal infection.