Mechanistically, frequent mutation of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), and overexpression of HER2 in breast cancer downregulated the ΔNp63α (a predominant p63 isoform) which disrupted the transcription and expression of AMPKα1 and subsequently inhibited the expression of E-cadherin [45]. This evidence concerns the gene PRKAA1 and breast carcinoma.