To determine whether NF-κB is the mediator responsible for TNF-α–induced GPRC5A repression, we examined the role of TNF-α in cancer cells treated with either RelA/p65 (subunit of NF-κB) knockdown by small interfering RNA (siRNA) or overexpression of dominant-negative inhibitor IκBα S32/36A mutant (IκBα-AA). The gene discussed is GPRC5A; the disease is cancer.