Recent efforts by the Centers for Disease Control and Prevention (CDC), the US Food and Drug Administration (FDA), and state authorities have led to the determination that vitamin E acetate (VEA) is strongly associated with e-cigarette or vaping product use-associated lung injury (EVALI) (1). VEA has been found in nearly all patient lung fluid samples analyzed and not observed in lung fluid from healthy cohorts. Despite strong evidence linking VEA to EVALI, its putative role as a causative agent has yet to be determined. To address the key issue of whether VEA is a just marker or a significant mediator of EVALI, Wu and O’Shea (2) report in PNAS that VEA reacts when aerosolized with an e-cigarette to produce the highly toxic gas ketene. Confirmation that VEA-derived ketene is a causative agent of EVALI must await rigorous clinical investigation. However, Wu and O’Shea (2) have in the meantime uncovered a compelling lead