Aromatase inhibitors (AI) are a novel adjuvant endocrine treatment for estrogen receptor (ER)-positive, postmenopausal breast cancer. They function by inhibiting the aromatase enzyme that converts androgens into estrogens. AIs have demonstrated excellent efficacy in clinical trials and have shown supremacy over Tamoxifen. However, prolonged use of AIs can lead to acquired resistance. This resistance is characterised by aberrant ER signalling and crosstalk with growth factor pathways. CyclinD1 is currently being investigated in the lab in an AI resistant breast cancer cell line (Let-R) and there is evidence of differential gene expression when compared to classical genes such as pS2. In Let-R cells, cyclinD1 expression appears to remain estrogen regulated. It is thought that this is not solely regulated through ER but through estrogen signalling to c-jun N-terminal kinase (JNK). This study aims to characterise the Let-R cell line created in the lab and to optimise an ERα knockdown in Let-R cells.