Statins have well established efficacy in reducing morbidity and mortality from coronary artery disease in both the primary and secondary setting (1,2). This is almost certainly achieved by reduction in plasma LDL levels and other purported circulatory/anti-atherosclerotic effects (3). Beyond its therapeutic value in cardiovascular disorders, there is now emerging interest in developing statins as an anti-cancer agent. Inhibition of 3-hydroxy-3-methylglutaryl CoA reductase by statins impede the rate-limiting step of mevalonate pathway leading to reduced levels of mevalonate and its downstream products which are important in cellular homeostasis, cell signalling, protein synthesis and cell cycle progression. Growth inhibitory signals exerted by statins in cancer cell lines and tumor-bearing animal models further support potential pro-apoptotic, anti-proliferative and anti-invasive properties (4). Aberrant regulation of cholesterol homeostasis has also been associated with cancer pathogenesis. Interestingly there has been recent genetic link identified between cholesterol and cancer risk further providing rationale for cholesterol targeting as a therapeutic or preventive strategy. Smith et al. (5) demonstrated anti-cancer function of cholesterol exporter ABCA1 (ATP-binding cassette transporter AI) in cell lines. Defective cholesterol efflux following suppression of ABCA1 gene expression in response to oncogenic mutations or loss of function mutation has been implicated in malignant cell transformation. ABCA1 deficiency allows for elevated mitochondrial cholesterol which supports cancer cell survival.