As it is known that cancer is regarded as a chronic disease that produces an inflammatory pattern different from that of an acute disease model, and drawing together the independent evidence that (i) TF is the dominant coagulation factor within the tumor microenvironment [11]; (ii) complement components could be cleaved by coagulant factors [18,19,20]; and (iii) complement facilitates tumor progression [16], an attractive hypothesis arose that coagulation induced by tumor-derived TF within the tumor microenvironment may facilitate tumor progression via the activation of complement. The gene discussed is TF; the disease is neoplasm.