While these prior findings support the potential benefit of developing pharmacological agents that increase O-GlcNAcylation and thereby decreasing tau phosphorylation for the treatment of Alzheimer’s disease, our observations that α-synuclein accumulates in response to thiamet G suggest that such an approach may be detrimental to α-synuclein homeostasis. The gene discussed is MAPT; the disease is Alzheimer disease.