We speculated that SLC26A9 enhanced canonical Wnt signaling in CRC cells based on the following events: (i) it increased the expression of pc-Myc, Bcl2, CyclinD1 and Snail but decreased that of AIF, cleaved Caspase 9 and cleaved Caspase 3, ultimately resulting in suppression of caspase-dependent and caspase-independent apoptosis; (ii) Snail expression was upregulated to promote EMT transformation, and E-cadherin expression was downregulated to promote migration and invasion; and (iii) EMT, as a key regulatory factor of the CSC phenotype, provided clues to the nature of tumor heterogeneity. The gene discussed is AIFM1; the disease is neoplasm.