Retinoic acid receptor-γ (RARγ) agonism is a key factor in CD8 T-cell-mediated immunity to infectious pathogens. The lack of studies on the effects of RARγ agonists on in vivo tumor growth of triple-negative (TNBC) or HER2+ breast cancers make it necessary to investigate whether RARγ could play a critical role in T-cell-mediated immunity in these breast cancers, using novel RARγ nuclear agonists.

Retinoic acid (RA) is fundamental to maintain immune homeostasis. In this process, RA induces regulatory T cells and promotes tolerance, but depending on the conditions, RA may also promote inflammation and tissue damage.