Since it was previously shown that SAMHD1-deficient fibroblasts from patients with Aicardi Goutières syndrome (AGS), a rare inflammatory disease, had elevated dNTP pools associated with chronic DNA damage and up-regulation of interferon (IFN)-stimulated genes [54], it is possible that SAMHD1-deficient resolved epidermal keratinocytes also have elevated dNTP levels compared to never-lesional cells, which may lead to latent and persistent DNA damage and inflammation. This evidence concerns the gene SAMHD1 and Aicardi-Goutières syndrome.