Our finding that DGCR8 expression is robustly associated with severity of SA deviation in 22q11DS across age subgroups is consistent with this literature implicating DGCR8 as a key contributor to brain and behavioral phenotypes in 22q11DS, and suggests that DGCR8 hemizygosity may contribute to SA reductions by disrupting miRNA modulation of cell cycle regulation during early brain development in 22q11DS. The gene discussed is DGCR8; the disease is 22q11.2 deletion syndrome.