FGF23 and congenital rubella syndrome: Our results showed that the MAPK pathway was significantly activated in the kidneys of CRS mice, but there was no significant change on the calcineurin/NFAT pathway, while in cultured fibroblasts of NRK-49F cells, we noted that FGF23 exerted no significant influence on either MAPK or calcineurin-NFAT pathway, partially in agreement with a previous study showing that FGF23 cannot activate MAPK signaling pathway in the absent of Klotho [64].