By combining the evidence regarding the fact that CRMP2 is a CRC biomarker [15] and our finding that CRMP2 participates in lipid metabolism and deposits [18], it was logical to hypothesize that CRMP2 is implicated in the etiology of CRC-DM comorbidity through regulating glucose/lipid metabolism, as well as CRC pathogenesis and/or progression. Here, DPYSL2 is linked to colorectal carcinoma.