OBJECTIVES/GOALS: Breast cancer has an increased requirement for lipids. The sigma-2 receptor plays a critical role in the effective uptake of lipoproteins by forming a complex with the LDL Receptor. We investigate the role of the sigma02 receptor in modulating lipid uptake pathways in breast cancers, and how this can be leveraged as a viable therapeutic strategy. METHODS/STUDY POPULATION: CRISPR/Cas9 will be used to ablate TMEM97 in the MDAMB231 and MCF7 cell lines. This study seeks to identify pathways that are dysregulated upon TMEM97 knockout (KO) by characterizing RNASeq data to identify differentially expressed genes and perform pathway analysis. RESULTS/ANTICIPATED RESULTS: Knockout of TMEM97 in breast cancer cells is is expected to decrease lipid uptake. Treatment with statins in these knockout cells is expected to result in decreased cell viability and result in a quiescent cell population. DISCUSSION/SIGNIFICANCE: This is an important mechanistic study to understand the importance of lipid homeostasis in cancer cell proliferation and how it can be targeted to improve therapeutic anti-tumor strategies. Understanding the pathways that TMEM97 modulates is vital for therapeutic strategies to curb the proliferation of breast cancer cells.