We previously proved that the removal of IFNγ from AD CM by using IFNγ‐neutralizing antibody prevented microglial proinflammation and consequently improved the neural viability, which was clear enough in our in vitro model.[4b] We also revealed the microglial phenotype transition leading to neurodegeneration via Keap1‐Nrf2 axis by using Nrf2 KD MG or Nrf2 OE MG. The gene discussed is IFNG; the disease is Alzheimer disease.