This makes it difficult to sustain therapeutically effective concentrations within the tumor microenvironment, thus achieving limited enrichment of cDC1s.  Moreover, recent studies indicated that cDC1s can be inactivated or exhausted by the interaction between vascular endothelial growth factor (VEGF) and neuropilin 1 (NRP‐1) expressed on cDC1s.[23, 24, 25] Therefore, the antitumor activity of cDC1s relies not only on their adequate recruitment and differentiation but also on maintaining their activation state in the TME. Here, VEGFA is linked to neoplasm.