“…While pathogenetic mechanism of autosomal dominant polycystic kidney disease (ADPKD) might be different from that of CARC, it has been reported that hepatocyte growth factor (HGF) and its receptor, c-MET, to be involved in the formation of ADPKD [ 26 , 27 ]. In this regard, crizotinib is a dual c-MET and ALK inhibitor [ 10 , 15 – 17 ], but accumulating number of case reports demonstrated that crizotinib is associated with development of cystic lesions in the kidneys, liver, and pancreas [ 20 , 24 , 28 – 35 ]. While the mechanism of CARC formation remains to be defined, as proposed by Wiest et al [ 30 ], complete collection of the following information from the advanced NSCLC patients treated with crizotinib is recommended, that is, patient’s general information including age, gender, race/ethnicity, history of renal cysts; clinical information of primary including stage at diagnosis, genetic information, treatment history, treatment response, PFS; tyrosine kinase inhibitor-associated renal cysts including time to diagnosis, laterality, pathology, symptoms, complications, abnormalities in vitals and labs.…”