The most common molecular mechanisms in TS are maternal UPD 14 (accounting for up to 78% of TS patients), paternal microdeletions of 14q32.2 (9.8%), and primary epimutations (hypomethylation) of the MEG3/DLK1:IG-DMR (ranging from 11% to 60%) [56,57]. This evidence concerns the gene DLK1 and Timothy syndrome.