However, in humans, RNase H2 has been proposed to also have non-enzymatic activities, this is partly based on the fact that mutations in the genes coding for the human RNASEH2B and RNASEH2C, which disrupt protein-protein interaction functions and not catalytic activity, are linked to Aicardi-Goutiéres syndrome [51]. This evidence concerns the gene RNASEH2C and Aicardi-Goutieres syndrome.