There are several papers linking Ca2+-permeable TRP channels to NF-κB-mediated inflammatory reactions; suppression of TRPC1-mediated Ca2+ entry inhibited NF-κB activation, which is associated with immunosuppressive mechanism in helminth infections [34]; pharmacological inhibition of TRPM7 channel suggested its involvement in LPS-induced EC migration via the TLR-NF-κB signaling [37]; endotoxin-induced lung injury involves TLR4-mediated NF-κB activation in a manner dependent on TRPC6-mediated Ca2+ entry [21]. The gene discussed is NFKB1; the disease is helminthiasis.