CACNA2D1 and Intellectual disability: The loss-of-function frameshift nature of two of the three identified CACNA2D1 variants, together with our functional studies demonstrating a loss-of-function effect for the amino-acid substitution p.(Gly209Asp), confirm disease causation of homozygous and compound heterozygous CACNA2D1 variants, while also calling into question a causative role of monoallelic CACNA2D1 variants in intellectual disability, epilepsy and/or inherited arrhythmogenic diseases.