The remaining ∼10% of human cancers maintain telomere length via a recombination-dependent, alternative lengthening of telomere (ALT) mechanism (Bryan et al., 1997) that display a number of defining features, including heterogeneous telomere lengths, increased frequencies of telomere sister chromatid exchange (T-SCE), ALT-associated PML bodies (APBs), and extrachromosomal telomeric repeats (ECTR), which include C-rich (ss)circles (C-circles) (Murnane et al., 1994; Bailey et al., 2004; Henson et al., 2009; Cesare and Reddel, 2010). The gene discussed is GPT; the disease is cancer.