Increased neutrophil counts and elevated fibrinogen levels indirectly enhance venous thrombosis in mice with B cell deficiency.[13] In contrast, T-cell activation promotes platelet aggregation through increased cytotoxic T cells (CD8 + T) and T helper cells (CD4 + T) mediated by platelet GPIIb/IIIa, CD40L, and the lymphocyte integrin αM.[14] Decreased B-cell and T-lymphocyte subsets contributed to the hypercoagulable state of the patient. The gene discussed is CD4; the disease is Venous thrombosis.