One important paradigm of mitochondrial ROS production modulation states that high levels of mitochondrial membrane potential (ΔΨ_m) increase ROS generation in the respiratory chain. In a common project with the laboratory of Prof Cannon (The Wenner-Gren Institute, Stockholm, Sweden), we addressed this hypothesis on a model of brown adipose tissue (BAT) mitochondria, where ΔΨ_m is dissipated by the action of uncoupling protein 1 (UCP1). We compared the ROS production in BAT mitochondria isolated from wild-type mice or from UCP1−/− mice (with a high membrane potential) and found only ROS production supported by exogenously added succinate was affected by the presence of active UCP1. ROS production supported by any other tested substrate (including endogenously generated succinate) was not affected by ΔΨ_m. This indicates that UCP1 is not involved in the control of ROS production in BAT mitochondria, possibly indicating that also under other situations membrane depolarisation would not decrease physiologically relevant ROS production (Shabalina et al., Biochim Biophys Acta 1837: 2017, 2014)