In this sense, it has been suggested that in proteinopathies, where misfolded or toxic proteins accumulate in the nervous parenchyma, microglia engage in self‐antigen presentation (e.g., amyloid‐β or phosphorylated Tau) through MHC I/II, what favors the restorative profile of microglial cells (reviewed in Das & Chinnathambi, 2019). The gene discussed is MAPT; the disease is proteostasis deficiencies.