BTG3 and deep vein thrombosis: One suggested possible mechanism is that antiphospholipid antibodies induced by M pneumoniae infection result in a transient hypercoagulable state, because positive ANA and aCL-IgM were found in more than 50% of patients with M pneumoniae infection, especially M pneumoniae -associated thrombosis.[3,7] These findings suggest that the autoimmune inflammation caused by antiphospholipid antibodies plays a crucial role in the process of thrombosis.