The entire C-terminal region of histone-lysine-N-methyltransferase KMT2D (residues 4507-5537), which includes the ZF, PHD7, FYRN, FYRC, WIN and SET domains, is involved in binding to the WRAD complex (Dhar et al. 2012). Missense mutations in the C-terminal region of KMT2D, identified in Kabuki syndrome patients, affect its binding to the WRAD complex (Cocciadiferro et al. 2018, Lavery et al. 2020), consisting of WDR5, RBBP5, ASH2L and DPY30. While the impact of KMT2D truncating mutations on the WRAD complex binding has not been tested, they were shown to frequently result in KMT2D mRNA degradation through nonsense-mediated mRNA decay and contribute to haploinsufficiency (Micale et al. 2014).