Given the importance of known LZAP-binding partners in human cancer (for example, ARF, p38, Wip1, RelA, Chk1 and Chk2) and the dearth of knowledge concerning functional regulation of LZAP through protein–protein interactions or posttranslational modifications, it is also possible that LZAP may play opposing roles in tumor promotion depending on surrounding cellular environment and/or genetic defects co-existing in the tumor. This evidence concerns the gene CDKN2A and neoplasm.