ELAVL1 and kidney disorder: Although the mechanism of HuR overexpression and enhanced cytoplasmic translocation has not been investigated thoroughly in kidney diseases, the concurrently elevated mRNA expression and function of profibrotic and proinflammatory factors observed in present and previous studies, as the putative targets of HuR, suggest that excessive upregulation of HuR is causally linked to the onset or progression of kidney fibrosis and might provide us with the better molecular target to prevent or reverse kidney fibrosis.