In addition, GILZ and TLR2 may play a role in common barrier functions, since TLR2 activation has been reported to elicit protective effects on tight junctions in animal models of colitis [32], and exogenously administered GILZ protein reduced intestinal permeability and promoted ZO-1 expression in a dextran sodium sulfate (DSS)-colitis model [18]. The gene discussed is TJP1; the disease is colitis.