The selective killing of cDC1s by Tr1 cells presents a unique opportunity to enhance cancer immunotherapy by targeting this specific interaction. By understanding that HDVax-induced Tr1 cells are responsible for the inhibition of antitumor responses through the elimination of MHC-II tumor antigen-presenting cDC1s, we can develop strategies to disrupt this process. One approach could involve developing therapies that block the cytotoxic activity of Tr1 cells specifically towards cDC1s, thereby preserving the population of cDC1s within tumors. This preservation of cDC1s would lead to increased antigen presentation and activation of effector T cells, ultimately enhancing the immune response against the tumor. Additionally, utilizing techniques to selectively deplete or inhibit the generation of Tr1 cells in response to HDVax could prevent the suppression of cDC1s and promote a more robust antitumor immune response.