To determine if the PDGFRB/STAT3 pathway was essential to the pathogenesis of ARPKD fibrosis, we examined the effect of three inhibitors of the PDGFR tyrosine kinase (Crenolanib43,44, Sunitinib45,46, and Imatinib47,48) on the extent of ARPKD organoid fibrosis using three different methods: quantitative collagen immunostaining in whole organoids, and measurement of hydroxyproline and quantitative collagen mRNA assessment. The gene discussed is STAT3; the disease is autosomal recessive polycystic kidney disease.