However, NUGC-4 and SNU1 or Hela cells, expressing low levels of CEACAM1 or no CEACAMs, respectively, showed no significant changes in IL-8 secretion as well as the processing of p100 to p52 upon infection with HopQ-deficient H. pylori, indicating that efficient binding of HopQ to CEACAMs is necessary for the activation of these carcinogenic pathways (21, 22). This evidence concerns the gene CXCL8 and infection.