Indeed, several works have proposed a tumour suppressive role for SEMA3A, which has been reported to restrain tumour growth by hampering tumour angiogenesis.59 In PDAC, an NRP1-independent superagonist SEMA3A was used as vasculature normalising agent which demonstrated antitumour activity.60 Moreover, there are contradictory results on the effect of SEMA3A on recruitment and activation of TAMs. The gene discussed is SEMA3A; the disease is neoplasm.