We and others (14, 15) recently described perilipin 2 (PLIN2) as a marker of lipid droplets in tubular epithelial cells during kidney injury, and Mukhi et al. confirmed an upregulation of Plin2 after kidney injury in their mouse models, as well as a decrease in Plin2 expression after ACSS2 loss, further supporting the idea that inhibition of DNL can reduce lipid accumulation in kidney disease (4). This evidence concerns the gene PLIN2 and kidney disorder.