Our data extend previous findings by demonstrating that signals through CD30 D1 alone are sufficient to drive canonical and alternative NF-κB activation in cells that endogenously express CD30 and importantly that D1 signaling induces transcription of p21WAF1/CIP1 and impairs tumour cell division dependent on the canonical NF-κB pathway. The gene discussed is NFKB1; the disease is neoplasm.