Thus, targeting the biological function of LRP16 will provide the proof of principle for two understudied concepts in cancer therapy: (1) blocking subsignals, rather than total signals, as a means of impeding oncogenic NF-κB signaling and (2) targeting regulatory protein–protein interactions as a way to produce effective antitumor agents and to sensitize tumor cells to DNA-damaging cytotoxic therapies. Here, NFKB1 is linked to neoplasm.