Although overproduction of LPA and upregulation of the LPA2 receptor have been causally linked to cancer-associated inflammation and tumorigenesis in ovarian and breast cancers [16, 17]; thus far, it is not fully understood how TRAF6 is linked to the LPA2 receptor, and whether the function of A20 or CYLD in restricting LPA-stimulated NF-κB signaling is impaired in these cancers. This evidence concerns the gene CYLD and cancer.