To show a definitive role for α9β1 in SMC biology and neointimal hyperplasia in the comorbid condition of hyperlipidemia, we generated SMC-specific α9-deficient mice on apolipoprotein E–deficient (Apoe–/–) background (α9fl/fl SM22αCre+ Apoe–/–; hereafter for simplicity referred to as α9SMC-KO; Supplemental Figure 2A). This evidence concerns the gene IGKV1D-22 and hyperlipidemia.