Tamoxifen is a selective estrogen receptor modulator, used in chemotherapy and chemo-prevention of breast cancer. Diminution of the incidence of contralateral breast cancer, maintenance of bone density and diminution of the risks of contracting coronary diseases, are the beneficial effects associated to the use of tamoxifen. Adverse effects are endometrial pathologies, hepatic alterations and venous tromboembolic events. Tamoxifen distributes over the whole organism with a high apparent distribution volume (50-60 L/kg). The main site of tamoxifen biotransformation is the liver, but with a significant contribution of other tissues. Biotransformation is mediated by the cytochrome P450 system, especially by CYP3A4 and CYP3A5. Excretion occurs mainly through the bile. Binding to the estrogenic receptors generates interactions with regulatory sequences thus determining new response patterns. Besides its action through estrogenic receptors, tamoxifen has several other modes and sites of action. Carcinogenicity seems to be related to the cytochrome P450 mediated α-hydroxylation which leads to the formation of DNA adducts. Steatosis is said to be generated by modifications in lipid metabolism. In mitochondria, tamoxifen affects electron flow in the respiratory chain, stimulates ATP hydrolysis and impairs the membrane potential. Tamoxifen also increases lipid peroxidation, thus inducing oxidative stress. Further it also induces apoptosis via a mechanism that involves nitric oxide. Tamoxifen strongly incorporates into biomembranes where it interacts with both lipids and proteins. Different patterns of therapeutic associations have been investigated. The objective is to identify interactions and mechanisms, in the hope of discovering a safer treatment with less adverse effects.