Although reovirus is not a major viral pathogen in patients with acute asthma exacerbation, the study also showed that EphA2 suppressed the asthmatic inflammatory response in an ovalbumin-induced asthma murine model, suggesting that EphA2 functioned as a negative regulator of inflammasome activation upon reovirus infection by targeting epithelial NLRP3 and, thereby, guarding against an excessive, self-destructive immune response [138]. This evidence concerns the gene EPHA2 and asthma.