Although H. pylori have evolved mutant flagellin with low affinity for TLR5 to evade the immune system of the host, the H. pylori encoded protein cagL or cagY can still act as a flagellin‐independent TLR5 activator, and expression of TLR5 was correlated with active gastritis in murine models of H. pylori infection.46, 47. This evidence concerns the gene TLR5 and gastritis.