The present studies demonstrate that targeting eIF4A by zotatifin can robustly inhibit the translation of Sox4 and Fgfr1 in TNBC GEM models, resulting in not only the inhibition of cell proliferation, but also the induction of IFN-related pathways and remodeling of the tumor immune microenvironment. The gene discussed is EIF4A1; the disease is neoplasm.