The prospect of a potential SOX2‐EMT axis would not be surprising, considering that this axis is known to have central roles in the invasion and metastasis of several human cancers.24, 49, 50 For instance, SOX2 silencing in colorectal cancer cells induced mesenchymal‐epithelial transition, a reciprocal process to EMT, with marked changes in the expression of key drivers of EMT such as SNAIL.24 Consistent with these observations, our analyses indeed revealed reduced expression of EMT regulatory factors SNAIL and SLUG with SOX2 silencing. This evidence concerns the gene SNAI2 and colorectal cancer.