In vivo, PTX attenuates proteinuria and renal pathologies in several non-diabetic kidney disease models via modulation of signaling pathways or components triggered by cytokines (TNF-α, nuclear factor-κB, intercellular adhesion molecule-1, MCP-1 and CX3CL1/fractalkine), mitogens (platelet-derived growth factor, mitogen-activated protein kinase, phosphatidylinositol 3-kinase, Akt/protein kinase B and cyclin D1) and fibrogenic molecules (transforming growth factor-β, Smad3/4, connective tissue growth factor, collagen types 1 & 3, fibronectin and α-smooth muscle actin) [37, 78, 82–84]. This evidence concerns the gene AKT1 and kidney disorder.