As demonstrated above, loss of myeloid FX expression or FXa-PAR2 signaling improved tumor debris uptake and APC function by induction of the cGAS-STING-IFN-I axis (Figure 1E and Figure 3) and treatment with the direct FXa inhibitor rivaroxaban attenuated the formation of aggregates of immune-suppressive platelets with monocytes in tumor-bearing mice (Figure 5C). The gene discussed is F10; the disease is neoplasm.