Results from an in silico analysis demonstrated that the overexpression of PrPC under optimal culture conditions did not alter proliferation, resistance to cell death, and metabolism in colorectal cancer cell lines [436], and consequently, supported the hypothesis that the correlation between overexpression of PrPC, cancer malignancy, and MDR are actually results of a highly-stressed TME rather than outcomes being driven by PrPC overexpression. Here, PRNP is linked to colorectal cancer.