Previously, the Perkins group has shown that in cell lines, Checkpoint kinase 1 (CHK1) can phosphorylate the RelA C-terminal transactivation domain at Thr505, resulting in inhibition of tumour-promoting characteristics of NF-κB, including resistance to apoptosis, autophagy and cell proliferation/migration [14–17]. The gene discussed is CHEK1; the disease is neoplasm.