Thalidomide treatment in combination with alkylating agents in myeloma promotes prothrombotic conditions at the endothelium surface via a combination of mechanisms. Mechanisms include rapid apoptosis of myeloma cells leading to circulating tissue factor (TF), exposed TF by endothelium cells salvaged from apoptosis, increased circulating cytokines (eg, TNFα) with T-cell activation by antigen-presenting cells (APCs), and activated platelets in response to increased circulating cytokines.