In order to identify gene targets that can be co-targeted to enhance the growth-inhibitory effects of statins, we treated inherently fluvastatin-resistant MCF10.DCIS cells with fluvastatin and measured the levels of ACAT1/SOAT1 and ACAT2, two genes that we previously found to be significantly upregulated in statin-non-responsive mouse breast tumors relative to those in statin-responsive mice (statin-sensitive mammary tissues) [8]. This evidence concerns the gene ACAT2 and breast neoplasm.