It has been reported that thioredoxin-1 inhibitor Px-12 decreased cellular viability, induced morphological changes, increased ROS production, and ultimately induced renal tubular cell oxidative injury by activating the phosphorylation of c-Jun N-terminal kinase (JNK) and, consecutively, by increasing the expression of connexin 43 (Cx43) [178], a gap junction protein recently identified as key player in chronic kidney disease progress [179]. This evidence concerns the gene GJA1 and chronic kidney disease.