RNF56 (Cbl-b) directly binds MyD88, leading to degradation of MyD88 via poly-ubiquitination and the subsequent inhibition of MyD88-mediated inflammatory responses.196 A previous study has indicated that the deficiency of Cbl-b potentiates the sepsis-induced acute lung inflammation and mortality by enhancing the MyD88-dependent acute inflammatory response to sepsis.197 The RNF56 may be a new potential target for regulating the acute inflammatory response to sepsis. Here, MYD88 is linked to inflammatory response.