New findings suggest that the use of telomerase to induce proliferation in cultured cells for use in therapies may be associated with malignant changes. Collaborating scientists have introduced the gene encoding human telomerase reverse transcriptase (hTERT) into human mammary epithelial cells (HMECs) and studied the effects on expression of the “oncogene” c-myc. As expected, when hTERT was introduced in cells, c-myc expression was elevated; however, when hTERT was excised, overexpression of c-myc was maintained and telomerase activity also remained high (Nature 405, 755–756, 2000). Primary investigator David Beach of the Wolfson Institute for Biomedical Research (University College, London, UK) believes that “regulation of c-myc is most likely the key to utilizing this pathway for halting cell senescence.” He also maintains that there is another, earlier pathway involving the p16 tumor suppressor gene that must be studied to fully understand this system. Comparison of the p16 and c-myc regulatory pathways in cell lines other than HMECs should provide a better understanding of the role of hTERT in immortalizing cell growth.