DCLK1 and neoplasm: In PDAC, tumor-produced DCLK1-isoform2 functions as a novel initiator of macrophage polarization, able to cause tumor-associated M1 macrophages to shift towards the M2 type through the secretion of chemokines or cytokines, thereby impeding the growth of CD8+ T cells and the stimulation of granzyme-B, ultimately attaining an immunosuppressive effect [103].