CARD6, short for caspase recruitment domain family member 6, is a protein-coding gene. It contains a caspase recruitment domain (CARD) and is suggested to play significant roles in regulating NF-κB activation, which is involved in multiple biological processes like inflammation, apoptosis, and immune responses [3,4].

In SCI mouse models, CARD6 knockout significantly accelerated functional deficits, neuron death, and glia activation, while over-expression had the opposite effects. CARD6 knockout promoted apoptosis by enhancing Cyto-c release and Caspase-3 activation, and increased the inflammatory response by elevating pro-inflammatory cytokines via NF-κB signaling [1]. In collagen-induced rheumatoid arthritis (RA) mouse models, promoting CARD6 expression using adeno-associated virus (AAV) effectively attenuated the severity of arthritis, improved histopathological damage, and hindered bone erosion, by suppressing the TNFR1/TRAF2/NF-κB signaling pathway and reducing apoptosis [2].

In conclusion, CARD6 has anti-inflammatory and anti-apoptotic effects. The study of CARD6 knockout and over-expression mouse models reveals its importance in diseases such as spinal cord injury and rheumatoid arthritis, providing potential therapeutic targets for these diseases.