Dr. Lucas is a surgical and molecular pathologist with an interest in the relationship between chronic inflammation and the development of (1) malignancy, (2) metabolic dysfunction/insulin resistance, and (3) vascular disease/atherosclerosis. While each disease category is quite distinct, there are several underlying molecular mechanisms related to inflammation that link the three. In particular, his lab focuses on the role of an NF-κB signaling pathway that is activated by the “CBM signalosome,” a complex of three proteins (CARMA, Bcl10, and MALT1). Dr. Lucas originally studied this signalosome in lymphocytes, during his fellowship in the lab of Dr. Gabriel Nuñez at the University of Michigan. Here, he and his wife, Dr. McAllister-Lucas (also an ASCI member), found that the CBM signalosome mediates NF-κB activation in response to antigen receptor ligation and plays a key role in the adaptive immune response. Further, they explored how chromosomal translocations and point mutations that affect each of the three proteins underlie lymphomagenesis. Dr. Lucas’s work has more recently evolved to study the contribution of the CBM signalosome to G protein–coupled receptor (GPCR) signaling in endothelial cells, hepatocytes, and the cells of several carcinomas subtypes. The lab believes that the CBM signalosome, as a central “hub” for coordinating proinflammatory NF-κB signaling in response to a diverse array of ligand/receptor pairs, is a prime target for pharmaceutical development and that compounds designed to disrupt the signalosome could hold promise as therapeutics for several inflammatory-related diseases.