Abstract: Shelterin, including TRF 1, TRF 2, RAP 1, TIN2, TPP 1, and POT 1, is involved in the functioning of telomeres. Through interactions with some telomere-associated proteins, Shelterin proteins might directly or indirectly regulate the length of the telomere. Among those telomere-associated proteins, tankyrase can poly(ADP-ribosyl)ate TRF 1, and release it from the telomere, facilitating telomerase access to the telomere and inducing telomere lengthening. In most cancer cells, telomerase activity was largely upregulated, so in theory, inhibition of telomerase can induce shortening of the telomere and suppress the proliferation of cancer cells. The telomere shortening is a gradual process, and there is a time gap be-tween the inhibition of telomerase activity and the loss of the shortened telomere's ability to protect the end of the chromo -some. The shortened telomere may induce the efficacy of telomerase inhibition agents. Recent studies have shown that tankyrase is positively correlated with telomerase activity, and tankyrase inhibitors can induce cancer cell apoptosis by in -creasing telomere shortening. However, in some cancer cells relying on the mechanisms of ALT to maintain telomere length, tankyrase inhibition agents arrest the cancer cell growth by inhibiting the process of mitosis. In addition, the Wnt sig -nal pathway is another target of tankyrase inhibitors, largely because the tankyrase inhibitors can increase axin levels, which, in turn, induce the degradation of β-catenin, and eventual ly inhibi t cancer cel l prol i feration. Tankyrase inhibi tors might have strong anti-cancer abilities, considering the many signal pathways they target. Based on the recent studies of tankyrase, this article mainly focuses on the potential role of tankyrase in cancer therapy.