The inherent ability to reproduce linkage in an F2 cross between DA and BN provided sufficient evidence to us to conclude that arthritis regulation most probably stems from variations in Clec4b rather than Clec4e. We identified a causative nonsense SNP in the Clec4b DA allele that causes a truncation of the DA allelic protein that is nonfunctional but with expressed transcripts. Here, CLEC4E is linked to arthritic joint disease.