Our ribosome profiling data and the existing evidence regarding NF-κB activity and mitochondria emphasize the importance of our proposed brain-specific translational control mechanism of mTORC1- or glutamate receptor-mediated, Raptor-dependent proteasomal degradation of deamidated 4E-BP2 during a critical period of postnatal brain development (Figure 6C), which could go awry in neurodevelopmental disorders such as ASDs. Here, NFKB1 is linked to neurodevelopmental disorder.