Our findings implicate many ASD candidate genes altered by de novo, inherited, or X-linked CNVs (e.g., SETD5, miR137, and HDAC9 [MIM 606543]; Supplemental Data section “Highlighted Genes”) or altered by both de novo CNVs and LoF SNVs (e.g., RIMS1, TRIP12, and DLL1; Figures 4B and 5). Taken together, our results suggest that rare variants affecting ASD risk in the population collectively encompass hundreds of genes. Despite this heterogeneity, many genes converge in interconnected functional modules, providing diagnostic and therapeutic targets.