The major findings of the present study include the following: 1) the therapeutic potential of KEN for AD is expanded by impeding amyloidogenesis, in addition to inhibiting CDKs/GSKs that are implicated in Tauopathy;[29, 45] 2) the metabolic enzyme SHMT2 moonlights as the 5′UTR‐targeted RBP, and directly links OCM with amyloidogenesis through ADAM10 translation initiation; 3) GAGGG motif that acts as TIE highlights an important mechanism of SHMT2‐centered RNA processing in the pathophysiology of AD. The gene discussed is ADAM10; the disease is Alzheimer disease.