The most obvious explanation is that SEMA3F stimulates the TGFβ pathway, but another possibility can coexist with this first pathway in an in vivo tumor context, i.e., that the induction of MMP2, and MMP14 by SEMA3F, which have been implicated in the proteolytic cleavage-mediated activation of the TGFβ signal [58, 84], might occur, thus triggering the EMT program. The gene discussed is MMP2; the disease is neoplasm.