In human cells, the nuclease angiogenin mediates tRNA cleavage at the anticodon loop.11,12 This leads to generation of tRNA halves, whose level is elevated under cellular stress5 and in hormone-dependent cancers.13 Consequently freed 3′- and 5′-tRNA halves can form nicked structures that gain stability in body fluids.14,15 Other fragments, derived from the 3′-, 5′- ends or from the internal part of the tRNA—‘i-tRFs’—are produced by Dicer, angiogenin, RNase L and other—as yet—non-identified nucleases, whose actions determine the cleavage site in the tRNA molecule16 (Fig. 1). This evidence concerns the gene ANG and cancer.