Firstly, the ‘bacterial contamination hypothesis’, proposed by Khan et al. in 2016, suggests that the growth of endometriosis lesions is mediated by the LPS/Toll-like receptor 4 (TLR4) cascade due to high levels of Escherichia coli and therefore endotoxins in the menstrual efflux in peritoneal fluid [41]. The gene discussed is TLR4; the disease is endometriosis.