At the effector level of arthritis, apart from targeting effector molecules, like C5 [67,153] and its break down product C5a [65,154,155], receptors (FcRs [156], TLRs [157]), transcription factors [158,159]), and cytokines, using different strategies and drugs [160,161,162], methods for direct targeting of pathogenic IgG antibodies could be attractive and optimal for therapeutic applications. This evidence concerns the gene C5AR1 and arthritic joint disease.