However, we also highlight many recoding sites with undefined roles in neuronal development: p.R61G site in cyclin I (CCNI), peaking postnatally in the cortex but not in the cerebellum; p.K95R site in insulin-like growth factor binding protein 7 (IGFBP7), peaking postnatally in the cerebellum but prenatally in the cortex; p.I64M and p.S75G sites in signal recognition particle 9 (SRP9) peaking postnatally across all regions; a postnatal biased p.R580G site in SON DNA and RNA binding protein (RBP) (SON, the cause of ZTTK syndrome), among others (Figures 4A and 4B). Here, SON is linked to multiple congenital anomalies/dysmorphic syndrome-intellectual disability.