In effect, classic CdLS is more commonly seen from variants of proteins that regulate cohesin functioning (NIPBL, HDAC8), whereas non-classic or milder CdLS phenotypes are often attributed to variants in genes that encode structural units of the cohesin complex (SMC1A, RAD21, SMC3) or cohesin-associated proteins (ANKRD11, BRD4, and others). The gene discussed is RAD21; the disease is Cornelia de Lange syndrome.