Vangl2 functions as an adaptor to recruit ubiquitin ligase PDLIM2 and increase K63-linked ubiquitination on p65, which promotes the recognition of p65 by cargo receptor NDP52 and the autophagic degradation of p65, resulting in suppressing the production of proinflammatory cytokines and ameliorating sepsis. This evidence concerns the gene VANGL2 and Sepsis.