Notably, these correlations were independent of tumor histological subsites (Figure 4B), and are in line with previous reports suggesting that DCLK1 is involved in regulating of the NOTCH, KRAS, WNT, and TGFβ pathways to promote progression, EMT, and self-renewal in colorectal and pancreatic cancer cells (11, 13, 43, 44). Here, DCLK1 is linked to neoplasm.