The vSMC-specific knockout of TCF21 (transcription factor 21) in hyperlipidemic apolipoprotein E deficient (ApoE−/−) mice led to fewer fibroblast-like vSMCs in the protective fibrous cap of the atherosclerotic lesions.7 Moreover, high TCF21 expression is associated with decreased coronary artery disease risk in humans, possibly due to a more stable and fibroblast-like vSMC-rich plaque. Here, APOE is linked to coronary artery disorder.