To study mechanisms of STAT3‐activation in ARPKD, we therefore used a C‐terminal fragment of human FC that contains a short extracellular part, the transmembrane domain and the cytoplasmic tail (FCm; Figure S1D) to allow posttranslational cleavage of FC.2, 3. This evidence concerns the gene STAT3 and autosomal recessive polycystic kidney disease.