The hypothesis is that bacterial products, such as lipopolysaccharide, could activate TLR4-MyD88 axis in tumour cells followed by the production of proinflammatory cytokines, overexpression of antiapoptotic signals (XIAP and pAkt), and, finally, acquisition of chemoresistance by ovarian cancer cells [126]. This evidence concerns the gene MYD88 and ovarian carcinoma.