Structural modifications in the tacrine molecule served to develop novel candidates with MT activity against some AD hallmarks (β-amyloid deposition, tau protein hyperphosphorylation, N-methyl-D-aspartate-receptor-related excitotoxicity, AChE, BuChE, MAO-A, MAO-B, secretases) (Table S1). The gene discussed is ACHE; the disease is Alzheimer disease.