In previous studies of a murine lupus model, the selective deletion of MyD88 from B cells in MRL/lpr mice [29], dendritic cells in Lynflox/floxCd11c-cre+ mice [30], and complete deletion of the MyD88 gene in MRL/lpr mice [31] also prevented the generation of ANA antibodies and resolved the glomerulonephritis phenotype, but not the dermatitis phenotype. Here, MYD88 is linked to skin disorder.