data across hiPSC lines, patients, and laboratories. The above mentioned study 144 has also hypothesized that the Wnt signalling pathway, which when elevated causes excessive proliferation of NPCs 145,146, is paradoxically reduced in ASD with macrocephaly, and somehow this is related to the aberrantly increased proliferative activity, as agents that increased the canonical b-catenin/BRN2 cascade normalized cell proliferation. Further support for an involvement of this signaling pathway in ASD is provided by the observation that ASD patients have mutation in CHD8, a negative regulator of canonical Wnt signalling pathway 17,147–149.
