Conversely, the ectopic overexpression of LRP16 in C33A cells, in which the endogenous expression level of LRP16 is lower than that observed in other detected tumor cells (Supplementary Figure S2K), enhanced the phosphorylation of IKKβ (Figure 2G), the recruitment of NF-κB to the nucleus, the damage-dependent induction of the activity of NF-κB-dependent luciferase reporter gene and promoted cell growth/survival after DNA damage (Figure 2H and I and Supplementary Figure S2L–S2N). The gene discussed is MACROD1; the disease is neoplasm.