As we were unable to access samples collected during such clinical trials, the initial indication of an active involvement of tumor immunity stems from the retrospective analysis of archival breast cancer tissue from MMTV-PyMT mice, in which neoadjuvant ALK1-Fc monotherapy promotes a proinflammatory environment, with a markedly increased expression of Cd3 and Cd4, as well as factors like Ifng (encoding for interferon-γ) and Cd40l. This evidence concerns the gene ALK and neoplasm.