For example, a groundbreaking study of the effects of PROTACs on Alzheimer’s disease was successful in 2016 and demonstrated that TH006 abolishes the activity of tau by recruiting von Hippel–Lindau (VHL) E3 ligase, Subsequently, different groups developed Tau-Keap1-CPP, QC-01-175, and C004019 PROTACs using Keap1, CRBN, and VHL E3, respectively, as ligases to target the degradation of tau in Alzheimer’s disease models. The gene discussed is KEAP1; the disease is Alzheimer disease.