As expected, in our study high risk DCIS (high grade, comedo type necrosis, hormonal receptor negativity and HER2 positivity) showed a higher degree of genomic instability represented by an increased burden chromosomal gains and losses and the presence of deleterious/missense TP53 mutations.70 In general, genomic instability leading to high risk DCIS lesions might promote T cell activation (CD3 and CD4) and recruitment of regulatory T cells (FOXP3) as suggested by our data. The gene discussed is NR4A1; the disease is ductal breast carcinoma in situ.