In this context, treatment of MM cell lines and patient derived primary MM cells with various JAK1/JAK2, JAK2 and JAK pan specific inhibitors (e.g. INCB16562, CYT387 and TG101209) has been shown to inhibit cell proliferation. Furthermore, JAK inhibitors have demonstrated synergistic activity with established anti MM therapies such as melphalan and bortezomib (CYT387) or melphalan, bortezomib and dexamethasone (INCB16562), in both MM cell lines and patient derived primary MM cells. Sensitization of MM cells to dexamethasone in response to JAK inhibitors may occur through crosstalk between the JAK/STAT pathway and glucocorticoids. In this regard, dexamethasone treatment has been shown to increase STAT3 and the pro survival factor phosphatidylinositol-3 kinase (PI3K) levels in melanoma cells; in turn, PI3K was found to increase STAT3 levels. Prolonged exposure to dexamethasone results in resistance, which could be overcome, at least in part, by JAK/STAT inhibition.