By screening 31 etiological SATB2 missense variants using cell-based experiments (Figures 1 and 4), we show that missense variants associated with SAS may have distinct pathogenic mechanisms, with the majority showing effects consistent with a partial LoF, a subset causing an increase in SATB2 function, and a small set of variants not mapping to either of these two functional groups. This evidence concerns the gene SATB2 and SATB2 associated disorder.