When a mouse model deficient in CNTNAP2, FMR1, and SHANK3 was compared with an environmental model of a neurodevelopmental disorder in which mice were exposed to maternal immune activation during embryonic development, it was demonstrated that interleukin (IL)-17a production during inflammation directly affects the nervous system to improve the expression of social behavioral deficits (Reed et al., 2020). This evidence concerns the gene IL17A and neurodevelopmental disorder.