Abstract
Advances in lineage-tracking techniques have provided new insights into the origins and fates of smooth muscle cells (SMCs) in atherosclerosis. Yet new tools present new challenges for data interpretation that require careful consideration of the strengths and weaknesses of the methods employed. At the same time, discoveries in other fields have introduced new perspectives on longstanding questions about steps in atherogenesis that remain poorly understood. In this article, we address both the challenges and opportunities for a better understanding of the mechanisms by which cells appearing as or deriving from SMCs accumulate in atherosclerosis.