This activation of AMPK in response to DNA damage and its involvement in key mechanisms of DNA repair may help to explain why amplification of AMPK occurs in some cancers with loss-of-function mutations in TP53, since overexpression of AMPK may be able to compensate for the increased sensitivity of p53-null tumours to DNA damage, thus increasing survival of the tumour cells. Here, PRKAA2 is linked to neoplasm.