Moreover, both in vitro models of oxidative stress and in vivo models of cerebral ischemia have shown pharmacological inhibition of RIPK1 with Necrostatin-1 (Nec-1) significantly attenuates neuronal necroptosis, supporting its therapeutic potential in reducing neuroinflammatory damage (88, 89) (Figure 5). The gene discussed is RIPK1; the disease is brain ischemia.