This problem is important, as LDs store lipids as metabolic fuel and membrane lipid precursors2–4, and is relevant to human diseases, as mutations of LD proteins are linked to metabolic diseases, such as fatty liver disease (for example, PNPLA3 (refs. 5,6) and HSD17B13 (ref. 7)) or lipodystrophy (PLIN1 (ref. 8) and PCYT1A9). Here, HSD17B13 is linked to metabolic disease.