Epimutations and microdeletions that affect the paternally methylated ICR, or the promoter of the MEG3 polycistron, are causally involved in two congenital imprinting disorders: Temple Syndrome (TS14, OMIM 616222) and Kagami-Ogata Syndrome (KOS14, OMIM 608149) [83,86,87,88]. Here, MEG3 is linked to motor developmental delay due to 14q32.2 paternally expressed gene defect.