NOD1 induction has been demonstrated to have a significant role in inducing inflammation in vitro49–51, and murine studies have linked both receptors to Endoplasmic Reticulum Stress-Induced Inflammation during chlamydial infection and NOD1/2-deficient mice exhibit a reduction in clearance rates52,53, though it is presently unclear if these phenotypes are associated with ligand-dependent or ligand-independent NOD1/2 signaling54. This evidence concerns the gene NOD1 and chlamydia trachomatis infectious disease.