NFKB1 and diabetic kidney disease: Cellular and molecular experiments have shown that disturbed mitochondria function and endoplasmic reticulum stress, as well as abnormal activation of intracellular signaling pathways including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway, have found to be integrally associated with diabetic kidney disease [14,25,26].