However, it is well‐documented in the literature that dysfunctional adipose tissue and resident macrophages function as an endocrine organ, producing pro‐inflammatory cytokines that directly act on tumors (van Kruijsdijk et al., 2009), and more detailed insights for how the B6.Rag1−/− DIO mouse model system likely parallels human physiology in this regard came to light when we applied genomewide analysis to evaluate the greater impact of DIO on TNBC tumor gene expression. The gene discussed is RAG1; the disease is neoplasm.