In RCC cells, sunitinib triggers a TRAF2-mediated NF-κB survival signaling pathway and a PERK-driven endoplasmic reticulum (ER) stress response, which may lead to resistance to sunitinib in RCC patients, and NF-κB inhibition restores the sensitivity of RCC cells to sunitinib [51]. This evidence concerns the gene NFKB1 and renal cell carcinoma.