The HBP is activated in a Kras-dependent manner in PDA via transcriptional regulation of Gfpt1 (Ying et al., 2012), and it is similarly elevated in numerous cancers to provide a diverse set of functions, including the regulation of proliferation, survival, angiogenesis, and metastasis (Akella et al., 2019). The gene discussed is GFPT1; the disease is Patent ductus arteriosus.