Interestingly, the study of genistein effects on serum-, E2-, and EGF-stimulated cell growth has revealed that EGF-R was not targeted by genistein at cytostatic concentrations in breast and prostate cancer cells, and only cytotoxic concentrations (more than 50 μg/ml) achieved a noticeable inhibition of EGF-R tyrosine phosphorylation (88, 89). Here, EGFR is linked to prostate cancer.