In addition, TLR7 is the crucial driver in SLE, which regulates the GC of B cell and the production of autoantibodies.[20] And the TLR7Y264H variant, one TLR7 variant that could enhance TLR7 signaling, drives the increased senescence-associated pheno-type, including the accumulation of ABCs (B220+ CD21– CXCR5-CD19high CD11c+) and GC B cells (CD19+ CD95+ BCL6+) in SLE.[21] These data suggested that TLR7 is an important upstream driver of MyD88 dependence in human SLE, causing accumulation of ABCs. Here, MYD88 is linked to systemic lupus erythematosus.