In vivo, inhibitory signaling downstream of the FcγRIII [inhibitory ITAM (ITAMi) signaling] has been implicated in the IVIg-dependent reduction of TNFα and MCP-1 in a unilateral uretral obstruction nephritis mouse model; and FcγRIIB has been implicated in IVIg's anti-inflammatory activity in a mouse model of intracerebral hemorrhage, although IL-10 levels were not measured (41, 42). The gene discussed is IL10; the disease is intracerebral hemorrhage.