In this regard, it is of great interest that several studies have already demonstrated that KAT2B and KAT3B are involved in the modulation of NF-κB activity [43] and are required to co-activate p65-dependent transcription to activate several NF-κB-regulated inflammatory genes, known to be involved in cardiovascular disease, such as eotaxin, GM-CSF (granulocyte-macrophage colony-stimulating factor), and TNFα [44]. Here, NFKB1 is linked to cardiovascular disorder.