Subsequent experiments demonstrated that the expression of the fibrin(ogen) receptor integrin αMβ2 on myeloid cells alone was not sufficient to promote homing to metastatic tumor cells in the lungs of pFN-deficient C57BL/6-Fn(fl/fl)Mx-Cre+ mice, even though pFN-deficient mice exhibit no obvious clotting defects and generate clots around metastatic tumor cells to the same extent as pFN-competent wildtype mice [14,28]. The gene discussed is FN1; the disease is neoplasm.