Viau A, Baaziz M, Aka A, et al. - Given autosomal dominant polycystic kidney disease (ADPKD) results from the inactivation of the ciliary proteins polycystin 1 or polycystin 2, and despite a critical role of both signaling by primary cilia and interstitial inflammation in the disease, the reciprocal interactions between immune and tubular cells are not properly defined, so, researchers utilized conditional murine models including postdevelopmental ablation of Pkd1, Stat3, and cilia, and cultures of cilia-deficient or STAT3-deficient tubular cell lines, to determine how STAT3 intersects with cilia signaling, renal inflammation, and cyst growth. In ADPKD, repression of the expression of proinflammatory cytokines as well as restriction of immune cell infiltration was seemed to be brought about by STAT3. According to the findings, STAT3 was denied as a critical driver of cyst growth in ADPKD but its major role was suggested in the crosstalk between immune and tubular cells that shapes disease expression.