Interestingly, despite the high level of cell death that occurs following cerebral ischemia, one study reported that microglia have a more anti-inflammatory phenotype with higher expression of CD206, IL10, YM1/2, TGFB, ARG1, and CCL22 in the first 3 to 5 days following stroke, with a transition to higher expression of pro-inflammatory genes CD16, CD32, and NOS2 at 7 and 14 days post-stroke [131]. The gene discussed is TGFB1; the disease is stroke disorder.