Notably, GPR43 knockdown in Aβ1–42-treated cells resulted in dysregulation of apoptotic mediators, showing elevated CypD expression (1.29 ± 0.07 in AD/Si-GPR43 vs. 1.03 ± 0.03 in AD/Si-CON and 1.0 ± 0 in AD; p < 0.05; Fig. 7F) and increased BCL-2 levels (0.68 ± 0.05 in AD/Si-GPR43 vs. 1.01 ± 0.02 in Si-CON and 1.0 ± 0 in AD; p < 0.05; Fig. 7G). The gene discussed is FFAR2; the disease is Alzheimer disease.