In summary, our in vitro data support the notion that WEE1 inhibition alone may not provide a clinical advantage for PDA patients with mutations specifically in FANCC, FANCG, and BRCA2. We were able to validate these findings by silencing FANCD2 and BRCA2 in DDR-proficient PDA cells. The gene discussed is WEE1; the disease is Patent ductus arteriosus.