Moreover, a BRCC3 inhibitor or genetic deficiency of Abro1, a scaffolding protein with an essential role in the deubiquitinase activity of BRCC3 (20) was shown to reverse increased atherosclerosis and reduce neutrophil extracellular trap formation (NETosis) in atherosclerotic plaques of mice with macrophage cholesterol accumulation due to defective cholesterol efflux. Here, BRCC3 is linked to atherosclerosis.