A previous report indicated that PGAM1 promotes cell migration independent of its metabolic activity mainly through interaction of residues 201–210 with ACTA2 in breast cancer cells.[10] We aimed to distinguish whether this decrease in AKT expression is mediated by canonical metabolic activity or noncanonical PGAM1 activity related to its interaction with ACTA2. Here, ACTA2 is linked to breast carcinoma.