Oncogenes and tumor suppressors are equally altered in PDA, and recent NGS studies have shown the enormous complexity in the number of molecular alterations present in the PDA that range from somatic mutations (KRAS, TP53, ARID1A, TGFBR2, RREB1 and PBRM1), germline alterations (BRCA1, BRCA2, ATM and PALB2) and changes in copy number with gains (c-MYC, ERRB2 and KRAS) and losses (CDKN2A, SMAD4, ARID1A and PTEN). This evidence concerns the gene PTEN and Patent ductus arteriosus.