Since BTBR mice are currently a promising model for understanding the mechanisms that could be responsible for the pathogenesis of autism, we also examined the activity levels of NF-κB(p65) in the cerebellum and frontal cortex of BTBR mice and B6 mice (control) by determining the NF-κB(p65) phosphorylation on Ser 536 with an ELISA assay. Here, NFKB1 is linked to autism.