A previous study highlighted the importance of clinical history and visuospatial function assessment, rather than spontaneous extrapyramidal signs (EPS), in differentiating DLB from AD in early stages.71 While their approach focused on clinical features, our proteomic analysis revealed that AD and DLB share highly correlated profiles (r = 0.78) and similar dysregulated pathways, such as microglial activation (APP, CCL3, CX3CL1) and neuronal processes (APOE, MAPT, MME, SNAP25, SNCA). The gene discussed is CCL3; the disease is Alzheimer disease.