Herbimycin A, a benzoquinonoid anasamycin antibiotic, has been shown to reserve the oncogenic phenotypes of p60v-srctransformed cells by the virtue of the inhibition ofsrcprotein tyrosine kinase. Furthermore, we previously demonstrated that herbimycin A displayed the antitumor activity on Ph1-positive leukemia cells andbcr/abloncoprotein-associated transformed murine hematopoietic cells with the transfection of a retroviral vector expressingbcr/abl. Herbimycin A showed preferential inhibition on thein vitrogrowth of Ph1-positive leukemia cells andbcr/abloncoprotein-associated murine hematopoietic cells through the inhibition ofbcr/abltyrosine kinase activity and the reduction of subsequent phosphotyrosyl proteins. Recently, from the view of investigating the oncogenic significance or of developing a future clinical application in malignancies, several developing agents targeted against oncoprotein have been tried. We reviewed the present progress in the mechanism of oncoprotein-targeted antitumor effects and focused on herbimycin A-induced antitumor activity on Ph1-positive leukemia cells.