Intriguingly, whereas mutations to positively charged residues within the SMARCB1-CTD disrupt binding to the nucleosome and result in severe intellectual disability93,94,98, we report two novel variants in the SMARCB1-CTD, D369E and R376K, in which a positive or negative charge is maintained, and which are phenotypically associated with less severe disease (Fig. 4a, red, and Supplementary Table 1), underscoring that defining chemical properties of distinct mutations, even within a given subunit domain, may inform intellectual disability severity and phenotypic outcomes. Here, SMARCB1 is linked to Intellectual disability.