Even though different explanations have been proposed over-time, the exact mechanism of action of the anti-tumor activity of BPs is still not well understood. Basically, BPs are mevalonate pathway inhibitors and one of the most intriguing hypothesis supporting their anticancer activity relies on the modulation of the mevalonate downstream metabolism. Biologically active mevalonate metabolites are involved in tumour cell proliferation, survival, invasion and metastasis. Moreover, there is evidence that selected cancer subtypes may present a more pronounced mevalonate activity, able of maintaining an aggressive phenotype. Indeed, the mevalonate pathway has deep impact on the function of YAP/TAZ, transcriptional regulators of tumour growth. Preclinical evidences, suggest that BPs are able to interfere with YAP/TAZ expression, via mevalonate pathway. This study addresses the clinical role of BPs in triple negative breast cancer (TNBC) patients selected by the level of mevalonate pathway regulation, namely the p53 expression.