Mechanistically, an ACAT1 blockade by small molecule inhibition or by genetic inactivation (A1B) was reported to offer multiple benefits to AD models including the following: (1) A1B increased the content of the neuroprotective oxysterol 24(S)-hydroxycholesterol in the AD mouse brain [27] and in the AD patient iPSC-derived human neurons [30]. The gene discussed is ACAT1; the disease is Alzheimer disease.