Triple negative breast cancer (TNBC) is a malignancy with very poor prognosis, due to its aggressive clinical characteristics and lack of response to receptor-targeted drug therapy. In TNBC, immune-related pathways are typically upregulated and may be associated with a better prognosis of the disease, encouraging the pursuit for immunotherapeutic options. A number of immune-related molecules have already been associated to the onset and progression of breast cancer, including NOD1 and NOD2, innate immune receptors of bacterial-derived components which activate pro-inflammatory and survival pathways. In the context of TNBC, overexpression of either NOD1 or NOD2 is shown to reduce cell proliferation and increase the in vitro clonogenic potential. To further investigate the pathways linking NOD1 and NOD2 signaling to tumorigenesis in TNBC, here, we undertook a global proteome profiling of TNBC-derived cells ectopically expressing each one of these NOD receptors