The observation that some dividing cells can maintain telomere length in the absence of telomerase led to the discovery of a telomerase-independent TMM called the ALT mechanism.28, 29 In contrast to telomerase activation, telomere lengthening by ALT most likely arises in cells at crisis, as extraordinary genome instability is a feature of ALT-positive tumours. The gene discussed is GPT; the disease is neoplasm.