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). Here, PGAM1 is linked to cancer.