PGAM1 interacts with ACTA2 mainly through residues 201–210 to facilitate cancer cell migration independent of its metabolic activity.[7] Here, catalytically inactive H186R and Δ201–220 mutants lacking ACTA2 association were individually transfected into cells with stable knockdown of PGAM1 (Figure S7E, Supporting Information). This evidence concerns the gene ACTA2 and cancer.