C1 effectively activated TFEB through direct binding, increased autophagy-lysosome activity, decreased amyloid pre-cursor protein (APP), APP C−terminal fragments (CTF−β/α), β−amyloid peptides, and tau aggregates respectively in 5xFAD, P301S, and 3xTg-AD mice, and also improved synaptic and cognitive function (Song et al., 2020). The gene discussed is APP; the disease is Alzheimer disease.