One of the major mechanisms of tumor escape is the inability of antigen presenting cells (APC), and specifically the most potent APC dendritic cells (DC), to induce potent antitumor immune response. The defects in APC are caused by the variety of tumor-derived factors. In this review we will discuss recent findings which indicate that the members of the family of signal transducers and activators of transcription (STATs), and more specifically STAT3, could be responsible for the abnormal DC differentiation and function in cancer. The different approaches to pharmacological regulation of this pathway and their effects on DC function and antitumor immune responses will be discussed.