Likewise, two of three reported Weaver syndrome-associated mutations in SUZ12 are nonsynonymous substitutions within its VEFS domain, a key functional domain for its association with EZH2 and EED, which, when deleted, abolishes the enzymatic activity of PRC2 (Højfeldt et al., 2018; Imagawa et al., 2018). This evidence concerns the gene EZH2 and Weaver syndrome.