Cell type-specific deletion of Tgfbr2 in myeloid cells, i.e., granulocytes and monocytes, in mice results in cerebrovascular inflammation in the absence of significant pathology in other tissues, culminating in stroke and severe neurological deficits, indicating a crucial anti-inflammatory role of TGFβ signaling in myeloid cells within the CNS [296]. The gene discussed is TGFBR2; the disease is stroke disorder.