ADAR1 edits the SenZ and SenZ-ability of RNA.

Some RNAs can assume a Z conformation, an unusual, left-handed turn. In this issue of Immunity, three studies report that mutations in the Zα-RNA binding domain of the adenosine deaminase ADAR1 are sufficient to induce autoinflammatory disease in mice, which models human Aicardí-Goutières syndrome, highlighting the important role of Z-RNA editing in limiting innate immune recognition of endogenous RNA.