SEMA4A and neoplasm: Specifically, Nrp-1 recruits PTEN (phosphatase and tensin homolog deleted on chromosome ten) to disrupt pAKT (phosphorylated protein kinase, strain AK, Thymoma), forms the semaphorin 4 A-neuropilin 1 axis and participates in the interaction of Tregs with immature DCs, thus strengthening TI-Treg function and limiting anti-tumor immunity, while it is dispensable for Tregs to maintain immune homeostasis [74, 98–100].