Interestingly, a recent article described CCL2/MCP-1 as being upregulated by aberrant Notch signalling in patients with non-alcoholic steatohepatitis, driving liver monocyte infiltration and fibrosis.56 The above suggests that the observed phenotypic associations in CADASIL could be of immunovascular origin; however, targeted mechanistic studies are needed to prove this. The gene discussed is CCL2; the disease is metabolic dysfunction-associated steatohepatitis.