Since the PDA cells did not express other members of the TGM family (SI Appendix, Fig. S10D), this residual CXCL12–KRT19 coating may have been generated by the clotting factor F13a1 that was present in all PDA tumors (SI Appendix, Fig. S10E) and may be produced by infiltrating myelomonocytic cells. Here, F13A1 is linked to Patent ductus arteriosus.