Recent studies have shown a complex thiol-dependent interaction between TXNIP and the inflammation-related pathway of progressive diabetic nephropathy [31], the interaction of NLRP3 and TXNIP being a significant signal of the formation of NOX4-derived NLRP3 inflammation in hyperhomocysteinemia-induced glomerular damage [32]. This evidence concerns the gene NOX4 and hyperhomocysteinemia.