DCLK1 and cancer: Therefore, we propose that the dual inhibitory effects of the C-tail and the transmission of this information to adjacent DCX domains, which control adaptive cellular phenotypes such as EMT in cancer cells (48), may make allosteric classes of DCLK1 inhibitor a preferred therapeutic option, especially if they can be tailored specifically towards DCLK1.1 or DCLK1.2, whose autoregulation is different in terms of the varied molecular details we have uncovered here.