Complex IIb is subsequently activated in both ischemia and hypoxia, contributing to the phosphorylation and association of RIPK1 and RIPK3.202–204 Within the complex formed by this association, mixed lineage kinase domain-like is further activated by RIPK3, which eventually leads to cell death.205 Concurrently, a cascade of inflammatory reactions, including secretion of pro-inflammatory cytokines, favors necrosis damage and exacerbates ischemic brain injuries.206. Here, RIPK3 is linked to brain injury.