we have presented proof that EGFR localization to lipid rafts fits with EGFR TKI resistance. More, lovastatin, a Hmg-coa reductase inhibitor, together with NB 598, a squalene monooxygenase inhibitor reduced cholesterol biosynthesis within the EGFR TKI resistant breast cancer cells. Moreover, lovastatin sensitized buy PF299804 EGFR TKI resistant breast cancer cells to gefitinib induced growth inhibition. Notably, this sensitization of EGFR TKI growth immune cells to gefitinib was determined to be synergistic for both NB 598 and lovastatin. Our data shows that lipid rafts supply a system to advertise survival and growth signaling in the existence of EGFR kinase inhibitors. Over-expression of EGFR is one mechanism where EGFR plays a role in cancer development. Actually, overexpression of EGFR occurs in glioblastomas, Cholangiocarcinoma breast, prostate, ovary, liver, kidney, esophagus, larynx, belly, colon, and lung cancers. This fairly ubiquitous over-expression shows that EGFR may be an attractive target for cancer therapeutics. Inhibitors of EGFR kinase action show clinical efficacy lung, pancreatic, colorectal, and head and neck cancers, nonetheless they have proven ineffective in treating breast cancers. We have provided evidence that EGFR expressing breast cancer cell lines differ in their response to these EGFR TKIs. Eight of thirteen breast cancer cell lines were found to be immune to EGFR TKI induced growth inhibition using equally cellular viability and proliferation assays. Particularly, SUM159, SUM229, BT20, BT549, HCC1937, MDAMB231, and MDA MB468 mobile lines had IC50 values for gefitinib above 10 uM and continued to multiply in the presence of just one uM gefitinib. These designations of resistance are consistent with previously published Decitabine molecular weight leads to other cancer types. As double negative breast cancers, which lack expression of estrogen receptor and progesterone receptor and do not contain HER2 audio egfr expressing breast cancers are usually characterized. For that reason, hormone therapy and HER2 targeted antibodies, which are presently in clinical use, are not effective in this population of breast cancer patients. Of the thirteen EGFR expressing breast cancer cell lines that were characterized herein for response to EGFR inhibitors, all thirteen were bad for estrogen and progesterone receptors, and lacked HER2 audio. Taken together, these data support the requirement for specific therapeutics for these triple bad, EGFR indicating breast cancers. Unfortunately, despite the expression of EGFR in multiple negative breast cancers, there is a disappointing lack of clinical efficacy of EGFR TKIs. Numerous elements have been proposed for resistance to EGFR TKI induced growth inhibition in other cancers, including strains in EGFR, EGFR freedom and alterations in downstream signaling pathways.