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). The gene discussed is ACSS2; the disease is kidney disorder.