In accord with the results of a few previous studies (56, 67), our finding supports a potential mechanism connecting inflammation to HER2/neu-negative breast cancer, in which pro-inflammatory markers trigger JAK/STAT signaling pathways, activating genes responsible for cell proliferation and angiogenesis, and those aberrant pathways then contribute to an immunosuppressive tumorigenic microenvironment, leading to more aggressive breast cancer such as basal-like tumors (13, 56, 67). The gene discussed is SOAT1; the disease is breast carcinoma.