Non-exertional severe heatstroke due to passive heat exposure promotes the production of a variety of pro-inflammatory mediators, such as IL-1β, TNF-α, IL-6, and high-mobility group box 1 (HMGB1), which cause an excess activation of leukocytes, endothelial injury, and coagulation disorders that lead to multiple organ dysfunction [20–22]. Here, IL1B is linked to blood coagulation disease.