It is known that A20 negatively regulates the transcription factor of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), i.e., through interacting with RIPK proteins, and it was shown that A20 is capable of suppressing the activation of the NF-κB in the experimental setting of the murine traumatic bone injury model, challenged with LPS as a stimulus (51). Here, NFKB1 is linked to injury.