Pharmacological inhibition of P2X4R in an animal model of stroke was shown to be protective by reducing the number of infiltrating pro-inflammatory myeloid cells and improved both acute and chronic stroke recovery by reducing the levels of interleukin-1 beta (IL-1β) and limited the blood brain barrier (BBB) permeability to the leakage of leukocytes into the infarct territory at 3-day post-stroke [103]. The gene discussed is P2RX4; the disease is stroke disorder.