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 (Major et al., 1985), may make allosteric classes of DCLK1 inhibitor a preferred therapeutic option, especially if they can be tailored specifically toward DCLK1.1 or DCLK1.2, whose autoregulation is different in terms of the varied molecular details we have uncovered here.