Restoration of mitochondrial function and metabolic flexibility (for instance, via PPAR agonists or novel metabolism-targeted drugs) might therefore hold therapeutic value in CRS Type 4; intriguingly, one study in a mouse CRS model identified PPAR-α downregulation in the heart as a critical mediator of dysfunction and showed that microRNA-21 (a known inhibitor of PPAR-α) was upregulated, linking a metabolic deficit to a regulatory microRNA that could be targeted [35,36]. This evidence concerns the gene PPARA and congenital rubella syndrome.