We found that the obese state upregulated ERα expression in a murine model of obesity-associated BC (Figure 1), and demonstrated contribution of Mφ, adversely-activated by obesogenic substances (e.g., SFA) through TLR4-dependent mechanism, to ERα upregulation in mouse/human BC cells (Figure 2 and Figure 3; Supplementary Figure S2). The gene discussed is TLR4; the disease is obesity due to melanocortin 4 receptor deficiency.