Loss of function of the PC1 and/or PC2 proteins leads to ADPKD through multiple signaling pathways and proteins, including the mentioned mTOR, JAK and STAT, but also planar cell polarity (PCP), Wnt, cyclic adenosine monophosphate (cAMP), G-protein coupled receptor (GPCR), cystic fibrosis transmembrane conductance regulator (CFTR), epidermal growth factor receptor (EGFR), mitogen-activated protein kinase (MAPK), cellular Ca2+, and the cell cycle [15]. Here, SOAT1 is linked to autosomal dominant polycystic kidney disease.