In neurodegeneration, such as Alzheimer’s disease [122], microglia persist in a pro-inflammatory phenotype characterized by sustained IL-1β, TNF-α, and ROS secretion, while deficiencies in TREM2 and Gas6–Axl signaling impair the clearance of β-amyloid and synaptic debris, thereby perpetuating neuroinflammation and cognitive decline [36,123]. The gene discussed is IL1B; the disease is early-onset autosomal dominant Alzheimer disease.