Some of the observed mouse phenotypes including growth retardation, craniofacial dysmorphisms, and weakness are similar to human patients with MORC2 mutations (18), while others are opposite (microcephaly versus macrocephaly), which might stem from the fact that patients carry heterozygous MORC2 mutations in the adenosine triphosphatase (ATPase) module resulting in apparent hyperactivation of HUSH silencing. This evidence concerns the gene MORC2 and microcephaly.