While it was perhaps counterintuitive to find enriched pathways in estrogen response, closer examination of the genes responsible for driving that overrepresentation have functions outside of estrogen response and known roles in TNBC, including SLC9A1, which is implicated in epithelial-to-mesenchymal transition in TNBC (58), FAM102A, which is differentially expressed in BRCA-mutated cancers (59) that tend to be triple-negative, and CDH1, which is linked to TNBC proliferation and invasion (60). This evidence concerns the gene EEIG1 and cancer.