Hypercholesterolemia was then induced with gain-of-function AAV-PCSK9 and WD feeding, as previously described.42 In this model, reversal of hyperlipidemia by a switch to standard laboratory diet feeding was shown to reduce monocytosis and to induce measures of plaque regression, as defined by reduced plaque size, reduced content of plaque macrophages (CD68+), and increased collagen content.42,43 Body weight and plasma cholesterol were monitored during the study (Figure 3B; Figure S3A and S3B). The gene discussed is CD68; the disease is Hypercholesterolemia.