Furthermore, PLIN5 acts as a scaffold in chaperone-mediated autophagy in HepG2 cells demonstrating that co-localization of heat shock protein 70 (Hsp70) and PLIN5 serves as a substrate allowing degradation of LD in cells under FA stimuli, which mimics NAFLD [12]. Here, PLIN5 is linked to metabolic dysfunction-associated steatotic liver disease.