Post‐stroke BHB therapy resulted in a substantial decrease in the expression of proinflammatory chemokines (CCL3, CXCL1, CXCL9, CXCL10), complement (C5/5a), cytokines (IFN‐γ), and myeloid cell activators (G‐CSF) in the ischemic hemisphere (Figure 4A,B; Figure S5A,B, Supporting Information). The gene discussed is CCL3; the disease is stroke disorder.