As a deubiquitinase, inhibition of UCHL1 inhibits lipid uptake by increasing the abundance of K48-polyubiquitin on CD36 and thereby blocking its activation, thus suggesting that UCHL1 may be a potential target for atherosclerotic therapy [44], which may provide a new insight into the protein degradation of CD36 in lipid-metabolism-related ophthalmic diseases with similar pathogenesis to atherosclerosis. This evidence concerns the gene CD36 and atherosclerosis.