While pre- and post-stroke blockade of P2Y1 by MRS2500 i.c.v. proved beneficial for stroke outcome in transient and permanent MCAO models [63, 64], the role of P2Y6 in stroke is still controversial: Pharmacological inhibition of P2Y6-mediated phagocytosis with MRS2578 on 3 consecutive days after tMCAO aggravated infarct size, brain atrophy, and neurological deficits [65]. The gene discussed is P2RY1; the disease is stroke disorder.