Furthermore, excessive type I IFN production via cGAS-STING activation has been implicated in further models of inflammation-associated coagulopathy, including cerebral venous sinus thrombosis [139] and acute lung injury [140], indicating a broad spectrum of conditions where there is a strong correlation between dysregulated type I IFN production and aberrant coagulation. This evidence concerns the gene STING1 and blood coagulation disease.