To examine pathophysiological aspects of STAT3 signalling in human ARPKD, we studied patient samples and found increased activation of STAT3 in human ARPKD cyst‐lining epithelia and both an increased expression and variably increased activation of STAT3 in human ARPKD kidney lysates (Figure 1A, Figure S1C, Suppl. The gene discussed is STAT3; the disease is autosomal recessive polycystic kidney disease.