They further reported in 2022 that the interaction between TMEM30A and βCTF was one of the important pathogenesis of Alzheimer's disease [20], which inhibited the physiological complex formation and activity of lipid flippase in SH-BACE1 cells, and the BACE1 inhibitor treatment recovered this interaction. This evidence concerns the gene BACE1 and early-onset autosomal dominant Alzheimer disease.