Inhibitors of apoptosis proteins (IAPs) are crucial mediators of cell death and immune signaling. While they were originally described for their role in apoptosis, recent studies have extended the function of several IAP members to cell death processes beyond apoptosis, such as necroptosis and pyroptosis. It is now generally recognized that IAPs influence inflammatory pathways, including those activated through the inflammasome and NF-kB transduction. While the connection between programmed cell death and inflammation has always been recognized, the characterization of IAPs has further bridged the two fields. These processes are critical for innate immune responses and are commonly employed by host cells to clear pathogenic microorganisms that are potentially encountered. As a consequence, a number of successful bacterial and viral pathogens have evolved mechanisms to manipulate the signaling cascades that regulate both host cell death and inflammation to favor their own survival and persistence. Here we discuss the roles of cIAP1, cIAP2 and XIAP in host cell survival and inflammation, and how this impacts microbial pathogenesis.