NFKB1 and breast carcinoma: Based on the IL1 pro-inflammatory circuit proposed to drive HER2-dependent tumorigenesis [62], we then define a chronic inflammation signature calculated as the average expression level of IL1A, IL1B, IL4, IL6, CXCL2, NFKB1, and STAT3. Interestingly, despite the high CD45 expression in HER2-enriched breast cancer (Fig. 11A), the chronic inflammation signature (Fig. 11B) as well as the expression of TNFA (Fig. 11C) and TGFB (Fig. 11D) is low or average in HER2-enriched breast cancer relative to the other molecular subtypes.