In primary somatosensory cortex dysgranular zone (S1DZ) neurons, IL‐17 suppresses neuronal activity, a potentially protective mechanism against autism‐like behaviors (repetitive actions, social deficits) associated with S1DZ hyperactivation [131, 133, 134], with IL‐10 counteracting IL‐17‐induced changes in excitability [131]. Here, IL17A is linked to autism.