Semaphorins were initially described as guidance molecules involved in growth cone migration but were further involved in developmental and pathologic processes including cancer [43–46], and SEMA3C is generally described as a tumor promoting semaphorin [45] Thus, both NRP2 and SEMA3C overexpression might facilitate TGF-β1 signaling and tumorigenesis, and targeting NRP2 and SEMA3C would be useful to reduce EMT. The gene discussed is NRP2; the disease is neoplasm.