Based on a previous report and current data, we suggest that ZIP8-mediated zinc influx into chondrocytes is important for OA pathogenesis by upregulating matrix-degrading catabolic enzymes26,27, while ZIP8 mediated RA pathogenesis primarily by modulating the functions of CD4+ T cells, such as Tem cell activation, including that of Th17 cells. This evidence concerns the gene CD4 and rheumatoid arthritis.