MAPK3 and Alzheimer disease: In AD, where microglial biology is likely a driver of pathogenesis, inflammatory stimuli, such as fibrillar amyloid, activate toll-like receptor 4 (TLR4), which then triggers the extracellular signal-regulated kinases 1/2 (ERK1/2)—the proteins that are central to microglial dysfunction (Chen et al., 2021).