MTOR and cyst: The classical hypothesis for cyst initiation is that, in addition to a germline inactivating mutation in one allele of the PKD gene, there is somatic inactivation (referred to as the second hit) in the other allele, causing a complete loss of polycystin expression in the cell [5]; this dysfunction disrupts calcium regulation, altering cell polarity, proliferation, apoptosis, and extracellular matrix remodeling, and activating several signaling pathways, including cAMP, MAPK, mTOR, and canonical Wnt pathways [22,23,24].