In the United States 1 in 8 women will develop metastatic breast cancer within their lifetime, accounting for nearly 30% of cancer diagnoses annually. The heterogeneity of breast cancer makes treatment of the disease a challenge, since no single therapy is effective for all subtypes. Recent developments in immunotherapy, notably checkpoint inhibition, has revitalized efforts to create therapies that help boost the immune response to solid tumors. A novel approach that may help improve immunotherapy response in breast cancer is the inhibition of highly abundant long noncoding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript (MALAT1). MALAT1, has been associated with the cancer progression of liver cancer, renal cell carcinoma, lung cancer and has been shown to be upregulated almost four-fold in breast cancer. Targeting of MALAT1 is made possible through the use of antisense oligonucleotides (ASO). Our laboratory has shown that knockdown of MALAT1 in several murine tumor derived cell lines also elicits an increase in the stress marker p-eIF2α, and DNA damage marker γH2aX. Thus, the targeting of MALAT1 may be a beneficial therapeutic to help increase the immune response to tumor cells, creating a tumor microenvironment more susceptible to checkpoint inhibition.