In humans, several single nucleotide polymorphisms (SNPs) of STING have been discovered.24 SNPs of STING have been shown to cause autoinflammatory diseases such as STING‐associated vasculopathy with onset in infancy25 and familial chilblain lupus.26 These SNPs are implicated in the dysregulation of host innate immune responses and inflammatory responses through a loss‐of‐function mutation or a gain‐of‐function mutation of STING. The gene discussed is STING1; the disease is vascular disorder.