Genetic or pharmacological inhibition of RIPK3 reduces HMGB1 release in pulmonary fibrosis and subarachnoid hemorrhage models [60, 61], and reduced HMGB1 signaling could indirectly contribute to improved functional outcome in CCI because of its role in IL-1 beta production via toll-like receptor signaling [62, 63]. Here, RIPK3 is linked to pulmonary fibrosis.