In conclusion, our data demonstrate that targeting NRP-1 in cancer, using antagonistic anti-NRP-1 Nbs that prevent the interaction with Sema3A, delays growth of CRC tumors and extends the survival through a shift in the MHC-IIhigh/MHC-IIlow ratio and an activation of CRC-specific CD8+ T cells. Here, SEMA3A is linked to cancer.