Using AD rat models, which were produced by daily intraperitoneal injection of AlCl3, they found that treatment with p38α inhibitors significantly reduced brain levels of pro-inflammatory cytokines (NF-κB, TNF-α, and IL-1β) and exerted notable histopathological improvement in cortical and hippocampal regions in the AD models [59]. The gene discussed is TNF; the disease is Alzheimer disease.