The prime function of the arterial smooth muscle cell (SMC) in adult individuals is to contract and relax, thereby regulating blood flow to target tissues. However, in several vascular diseases, arterial SMCs in the adult vessel undergo major changes in structure and function. For example, SMCs can take on properties that allow them to proliferate and migrate, to promote calcification, to undergo apoptosis, and to orchestrate other cell types to take on different properties. These altered SMCs are often viewed as vascular troublemakers. However, these responses can also be seen as an attempt of the SMC to mend a diseased blood vessel. The plasticity and diversity of SMC populations and the presence of SMC progenitor cells contribute to the growing complexity of SMC biology. In the past couple of years, several new mechanisms that allow SMCs to proliferate, migrate, promote calcification, and communicate with and respond to other cell types have been discovered. Much of this work has been published in ATVB , and some of that body of work is highlighted in this article. We emphasize areas that have generated substantial interest, including novel mechanisms governing SMC phenotypic switching, SMC progenitor cells, noncoding RNAs as regulators of SMC function and phenotype, novel mechanisms of cross talk between SMCs and other cells and differences in regulation of SMCs and other vascular cells. The arterial SMC exhibits an impressive potential for plasticity. SMCs have been known to exist in different phenotypic states for decades, and the switch from a quiescent contractile phenotype to a synthetic proliferative phenotype is thought to play an important role in cardiovascular disease (for a historical perspective1). Thus, switching to a synthetic phenotype is generally thought to enable SMCs to migrate and proliferate in atherosclerotic lesions,2 thereby forming a fibrous cap covering a core of …