The induction of apoptosis in target cells is a key mechanism for most anti-tumor therapies. Bufalin is acardiotonic steroid that has the potential to induce differentiation and apoptosis of tumor cells. Research onbufalin has so far mainly involved leukemia, prostate cancer, gastric cancer and liver cancer, and has beenconfined to in vitro studies. The bufadienolides bufalin and cinobufagin have been shown to induce apoptosis ina wide spectrum of cancer cell. The present article reviews the anticancer effects of bufalin. It induces apoptosisof lung cancer cells via the PI3K/Akt pathway and also suppressed the proliferation of human non-small celllung cancer A549 cell line in a time and dose dependent manner. Bufalin, bufotalin and gamabufotalin, keybufadienolides, significantly sensitize human breast cancer cells with differing ER-alpha status to apoptosisinduction by the TNF-related apoptosis-inducing ligand (TRAIL). In addition, bufadienolides induce prostatecancer cell apoptosis more significantly than that in breast epithelial cell lines. Similar effects have been observedwith hepatocellular carcinoma (HCC) but the detailed molecular mechanisms of inducing apoptosis in this caseare still unclear. Bufalin exerts profound effects on leukemia therapy in vitro. Results of multiple studies indicatethat bufalin has marked anti-tumor activities through its ability to induce apoptosis. Large-scale randomized,double-blind, placebo or positive drug parallel controlled studies are now required to confirm the efficacy andapoptosis-inducing potential of bufalin in various cancers in the cliniucal setting.