One previous study found that complete deletion of TMEM59 could reduce Aβ pathologies and rescue reduced levels of GluA2, a component of the α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA) receptor in the APP/PS1 AD model mice that carry the APP Swedish mutation and the PS1 ΔE9 mutation.13 The gene discussed is TMEM59; the disease is Alzheimer disease.