In conclusion, this study demonstrates that the exposure of mouse neocortical cells to triclocarban, used at environmentally relevant concentrations, induces AHR- and CAR-mediated apoptosis, disrupts the epigenetic status of the neuronal cells, and inhibits posttranslational protein modifications in terms of sumoylation which may substantiate a fetal basis of the adult onset of neurological diseases. Here, NR1I3 is linked to nervous system disorder.