Some cells can be immortal without expressing telomerase and are termed ALT (alternative lengthening of telomeres). ALT cells maintain telomere length by homologous recombination. While almost all human cancers express telomerase, it has been suggested (but never shown) that tumor cells might escape telomerase inhibition therapy by activating the ALT pathway. In this study Bechter et al. show for the first time the conversion of telomerase positive cells to ALT-like cells after inhibiting telomerase. There are few good markers fort the ALT phenotype. Bechter et al. also describe a new ALT marker: recombination between telomere sister chromatids (T-SCE) occurs with a very high frequency in ALT cells as well as telomerase positive cells with experimentally shortened telomeres. On the cover, the insert is a normal telomere staining pattern, where each end contains a red dot (indicating leading strands) and a green dot (indicating lagging strands) while chromosomes are blue (DAPI staining). In ALT cells with sister chromatid exchanges within the telomere, red and green dots localize on the same chromatid arm to give a yellow color. This T-SCE marker was present in the inhibition-resistant ALT-like cells. This technique should permit the identification of cells with recombinogenic telomere ends and will further help to identify telomerase independent mechanisms of telomere length control. For details, see the article by Bechter et al. on page 3444 of this issue.