Recent experimental and clinical data suggest the mammalian target of rapamycin (mTOR) kinase as a molecular switch balancing tubular proliferation, tubular maintenance and cystogenesis. However, most data have been derived from pharmacological inhibition of the pathway by rapamycin making it impossible to differentiate the precise and cell specific role of mTOR activation. We have now established a set of complementary transgenic mouse models that identify tubular cell autonomous mTOR signalling events as mediators of cyst initiation and cyst progression. The overall goal of this project is to understand the precise timing and the molecular interplay of mTORC1 dependent and mTORC1 independent signalling events regulating cystogenesis to identify a novel and innovative multi-target based treatment approach for ADPKD.