Periostin strengthened fibrosis and apoptosis in tubular epithelial cells by activating the phosphorylated-p38 MAPK pathway, facilitated vascular calcification through αvβ3/Wnt/β-catenin signaling, and accelerated inflammatory reaction by activating the β3/FAK/AKT pathway under NF-κB medication or mTOR complex 1 (mTORC1)-mediated inhibition of autophagy in CKD [87,88,93,94]. Here, PTK2 is linked to chronic kidney disease.