Interestingly, this PROTAC also mitigated mitochondrial fragmentation and oxidative stress when subsequently tested in SH-SY5Y cells treated with synaptic fractions from postmortem amyotrophic lateral sclerosis (ALS) patient brains that are enriched in mis-localized hyper-phosphorylated tau [102], revealing the potential of PROTACs in a tau co-pathology context. The gene discussed is MAPT; the disease is amyotrophic lateral sclerosis.