with ADHD compared to controls (P = 0.015, OR = 2.19, s.e. = 0.32). For comparison, there was no enrichment in rare synonymous variants in the third gene set (P = 0.59). When evaluating the 18 genes from the “credible gene set” individually, SORCS3 was nominally significantly (P = 0.008; Supplementary Table 16) enriched in rPTVs in ADHD cases when compared to a combined group of iPSYCH controls and gnomAD individuals (non-psychiatric non-Finnish Europeans; n = 58,121); this suggests that SORCS3 might be implicated in ADHD both by common and rare deleterious variants.
