Furthermore, lenalidomide treatment of CLL cells leads to an upregulation of several co-stimulatory molecules such as CD80 and CD86, and subsequently their recognition by and activation of the immune system while it impairs CLL migration via upregulation of CORO1B (Coronin, Actin binding protein) and reduction of RhoH expression, thereby impeding pro-survival CLL cell−microenvironment interactions [30,34,35,36,37]. This evidence concerns the gene CD80 and B-cell chronic lymphocytic leukemia.