RAC1 and cancer: Simvastatin treatment leads to increased levels of the unprenylated Ras homologue gene family, member A (RHOA), Ras-related C3 botulinum toxin substrate 1 (RAC1) and cell division cycle 42 (CDC42), which then leads to the activation of the downstream signalling cascade involving superoxide production, JNK activation and Bim-EL upregulation, demonstrating the tremendous potential of simvastatin to induce cancer cell death(Zhu et al. 2013).