The foundation for supporting Hsp90 inhibitor clinical trials came from the landmark finding that 17-AAG directly binds to Hsp90 instead of its client protein v-src tyrosine kinase, resulting in dissociation of Hsp90 from v-src kinase and degradation of the v-src oncogene product in v-src-transformed mouse NIH3T3 and PC3 human prostate cancer cell lines.56 This evidence concerns the gene HSP90AB1 and prostate cancer.