Similar results were found in xenograft tumors from mock knockdown and FERMT1 overexpressing GC cells: the protein levels of p65 and p-p65 were decreased in xenograft tumors formed from FERMT1 knockdown GC cells but were increased in xenograft tumors formed from FERMT1 overexpressing GC cells (Figure 5f), thus indicating that FERMT1 plays an important role in the activation of NF-κB signaling in vitro and in vivo. The gene discussed is NFKB1; the disease is gastric cancer.