Although not discussed by Kabeche and colleagues or in previous publications, the links between ATR and mitosis provide an explanation for how reduced ATR function and subsequent aneuploidy may underlie the neuronal cell loss during development that leads to microcephaly and cognitive dysfunction, the major clinical, pathological, and disabling features of Seckel syndrome: reduced ATR function results in aneuploidy that leads to neuronal apoptosis. This evidence concerns the gene ATR and Seckel syndrome.