IFNA1 and familial hyperaldosteronism: Their findings showed that FH inhibition induced the accumulation of fumarate, leading to the release of mitochondrial DNA (mtDNA) and mitochondrial RNA (mtRNA) respectively, which further increased the production of type‐I interferon (IFN) through activation of the DNA sensor cyclic guanosine monophosphate–adenosine monophosphate adenosine synthetase (cGAS) and RNA sensors toll–like receptor 7 (TLR7), retinoic acid–inducible gene I (RIG‐I), and melanoma differentiation–associated gene 5 (MDA5).