This immune evasion mechanism has since been recapitulated in a similarly engineered model of β-catenin activated HCC, where it was observed that aberrant β-catenin activation led to tumor resistance to anti-PD1 therapy and that reinstating the expression of CCL5, a chemokine that was downregulated in the β-catenin driven tumors, could restore tumor immune surveillance[22]. This evidence concerns the gene CCL5 and neoplasm.