Here, we set out to study how neoadjuvant anti-PD-1 and anti-CTLA-4 blockade affects Treg phenotype and function, and whether the potential activation of Tregs by ICB forms an obstacle for local and systemic anti-tumor immunity in ICB-unresponsive mouse models of primary and metastatic breast cancer. The gene discussed is CTLA4; the disease is neoplasm.