Kumar et al. (2015) demonstrated that selective expression of the proton-activated receptor GPR4 in chemosensory neurons of the mouse retrotrapezoid nucleus (RTN) is required for CO2-stimulated breathing. Genetic deletion of GPR4 disrupted acidosis-based activation of RTN neurons, increased apnea frequency, and blunted ventilatory responses to CO2. Reintroduction of GPR4 into RTN neurons restored CO2-dependent RTN neuronal activation and rescued the ventilatory phenotype. Additional elimination of TASK2 (KCNK5; 603493), a pH-sensitive K+ channel expressed in RTN neurons, essentially abolished the ventilatory response to CO2. Kumar et al. (2015) concluded that their data identified GPR4 and TASK2 as distinct, parallel, and essential central mediators of respiratory chemosensitivity.