In more detail, in HER2-overexpressing cancer cell lines, it has been shown that the serine/threonine kinase Akt is capable of phosphorylating p57 at Ser 282 or Thr 310, causing the cytoplasmic delocalization of the protein and proteasomal degradation, and highlighting that Akt activity results in the destabilization of p57 by accelerating its turn-over rate [48]. This evidence concerns the gene CDKN1C and cancer.