In line with these studies[39–42], our results showed that phosphorylation of ERK1/2 was significantly upregulated in AGS and BGC823 gastric cancer cells in response to famotidine stimulation (Fig. 4 A), while inhibition of ERK1/2 by U0126 was able to attenuated the promotion effect of famotidine on NLRP3 inflammasomes, leading to decrease IL-18 expression and LDH release determined by Elisa and western blotting(Fig. 4B-D). This evidence concerns the gene IL18 and gastric cancer.