Regarding ER activity, their analysis showed that FOXA1 and GATA3, major regulators of the ER transcriptional program [17], were differentially mutated in ILC compared to IDC, suggesting that different mechanisms of tumor progression relying on ER signaling exist between the two histological subtypes (FOXA1: 7% in ILC vs. 2% in IDC; GATA3: 5% in ILC vs. 13% in IDC). This evidence concerns the gene FOXA1 and neoplasm.