“…First, regions often implicated in ASD pathology more broadly (e.g. Ecker, Bookheimer, & Murphy, ; Stanfield et al., ) emerge in samples that include ASD + ID, with disruptions reported in frontal (Hazlett, Poe, Gerig, Smith, & Piven, ; Nordahl et al., ; Pardini et al., ; Riva et al., , ), striatal (Billeci et al., ; Riva et al., ), temporal (Boddaert et al., ; Hazlett et al., ; Piven, Arndt, Bailey, & Andreasen, ; Spencer et al., ), and cerebellar (Boddaert et al., ; Cascio et al., ; Jeong, Chugani, Behen, Tiwari, & Chugani, ; Riva et al., , ) regions (although for negative cerebellar results in ASD + ID, see Hashimoto, Murakawa, Miyazaki, Tayama, & Kuroda, ; Manes et al., ; Scott, Schumann, Goodlin‐Jones, & Amaral, ; Zeegers et al., ), as well as in the corpus callosum (Billeci et al., ; Egaas, Courchesne, & Saitoh, ; Haas et al., ; Manes et al., ; Spencer et al., ) and the amygdala–hippocampal complex (Dager et al., ; Schumann et al., ; Trontel et al., ; although see for a negative result; Zeegers et al., ). Second, it appears that the grey matter (GM) volumes and the WM structure are impacted in ASD + ID relative to TD controls, but clear patterns regarding the directionality and localization of these effects are difficult to ascertain in such a diverse literature.…”