We had previously shown that Acat1/Soat1 gene knock out (KO) in the 3xTg AD mouse model [61] reduced the mutant full-length hAPP, suppressed the level of Aβ [27], and diminished the levels of unphosphorylated mutant human Tau, but did not hyperphosphorylate the mutant human Tau (HPTau) [32]. The gene discussed is MAPT; the disease is Alzheimer disease.