In a recent study, we demonstrated that human urinary podocytes expressing APOL1 risk variants are characterized by lipid accumulation and mitochondrial dysfunction while treatment with an ABCA1 inducer or LXR agonist ameliorated lipid-mediated mitochondrial dysfunction [124], suggesting that inducers of reverse cholesterol transport may represent a new therapeutic targeting strategy for patients with APOL1-associated kidney disease. This evidence concerns the gene APOL1 and kidney disorder.