TNFSF4 and hepatitis C virus infection: In vitro experiments indicated that OX40L expression promoted OX40‐driven activation of Treg cells.119 In another study of patients with hepatocellular carcinoma, liver‐resident monocytes and macrophages expressed OX40L (in response to concurrent hepatitis C virus infection), which in turn promoted liver Treg cell expansion.120 Moreover, two studies identified an association between single nucleotide polymorphisms in OX40L and increased occurrence of breast cancer.121, 122