Over the past few years, we have witnessed numerous and continuing advances in our understanding of molecular mechanisms facilitating chronic rhinosinusitis (CRS). The current issue of the American Journal of Rhinology and Allergy contributes further to this area of study. Drilling et al. 1 characterizes the in vitro activity of a bacteriophage cocktail against Staphylococcus aureus biofilms, revealing its effectiveness in eliminating the organism from a substantial portion of clinical isolates in both planktonic and biofilm forms. Hwang and colleagues examine characteristics of H2S in CRS, illustrating its role as an important CRS-associated inflammatory mediator. 2 Continuing this trend of translationally relevant scholarship, Batzakakis et al. 3 and Topal et al. 4 respectively delineate the relationship specific adhesion molecules and reactive oxygen species have with nasal polyposis. 4