Wong et al. reported that LPS induces inflammation by activation of the store-operated calcium (SOC) channel and NF-κB/ERK1/2 pathway in gastric cancer cells [34]; SOC channel was also found to participate in LPS-treated astrocyte activation [35]; in macrophage, transient receptor potential melastatin-like 7 (TRPM7), a non-selective but Ca2+-conducting ion channel, regulates LPS-induced macrophage activation by promoting cytosolic Ca2+ elevations [36]. This evidence concerns the gene NFKB1 and gastric cancer.