In 2016, two groups respectively identified a surplus of linear ubiquitin linkages in humans due to homozygous variants in OTULIN that result in an autoinflammatory disease: OTULIN‐related autoinflammatory syndrome (ORAS, also known as otulipenia) (30, 31). This evidence concerns the gene OTULIN and autoinflammation, panniculitis, and dermatosis syndrome, autosomal recessive.