Strikingly, GLI2 overexpression strongly induced the mesenchymal markers ZEB1, VIM and basal-like marker KRT14 in YAPC cells and led to downregulation of epithelial markers E-Cadherin and ESRP1, and the transcription factor GATA6 - a putative regulator of the classical subtype of PDA (Collisson et al., 2011; Martinelli et al., 2017) and SHH in YAPC and HPAFII cells (Figure 3A; Figure 3—figure supplement 1A). The gene discussed is GLI2; the disease is Patent ductus arteriosus.