By resetting the level of MyD88 signalling in both infiltrating and resident kidney cells, SMAs such as 11a appear to act to suppress generation of pathogenic ANA and consequent immune complex-deposition and pro-inflammatory cell infiltration, responses which in concert drive IL-6-mediated lupus nephritis.7 Thus, such a drug-like compound, based on the safe, natural immunomodulatory action of ES-62 that has evolved over millennia to suppress aberrant, but not protective, inflammation, may provide the starting point for the development of novel therapies for SLE. The gene discussed is MYD88; the disease is lupus nephritis.