The largest family exome-sequencing study for TS to date (800 trios), also pointed to de novo mutations that contribute to TS risk (8, 70), implicating two high-confidence TS risk genes, WWC1 and CELSR3. On the contrary, focusing on common genetic variants, a large GWAS by Yu et al. (6) and follow-up studies showed that ligand-gated ion channel signaling, immune, cell adhesion, and transsynaptic-signaling processes are involved in TS (7). This evidence concerns the gene GLRA3 and Timothy syndrome.