To understand potential compensatory mechanisms in PDA, the authors conducted gene knockdown studies in AsPC-1 cells targeting the three enzymes involved in ornithine synthesis: OAT, ARG2, and GATM (glycine amidinotransferase), as well as the rate-limiting enzyme for polyamine synthesis, ornithine decarboxylase 1 (ODC1).4 Interestingly, silencing OAT, but not ARG2 or GATM, significantly reduced glutamine-derived ornithine synthesis and putrescine production. The gene discussed is OAT; the disease is Patent ductus arteriosus.