Of note, ectopic expression of LRP16 mutants (D160A or I161A), which was sufficient to significantly reduce its affinity for PAR, but not LRP16 wild-type (WT), in SW480 cells, dramatically sensitized the tumor cells to genotoxic stress-induced apoptosis, as conveyed by reduced cell viability and clonogenicity, in line with the indispensible role of the affinity of LRP16 for PAR in NF-κB activation and anti-apoptotic transcription (Figure 2—figure supplement 3D). Here, NFKB1 is linked to neoplasm.