In the study, we sought to determine whether the MVs, vectors of integrating all the proatherogenic factors in NVAF, could be endogenous CD36 ligands that transmit an activating signal to platelets to induce prothrombotic phenotype and whether the PMV‐CD36 complex is an effective target for treating NVAF‐related thrombosis. The gene discussed is CD36; the disease is Venous thrombosis.