While this study did not directly address the mechanism or cellular origin of the increased ASIC1a expression in vivo, our previous in vitro work in Fabry disease models (Salinas et al., 2020) showed that Gb3 and its derivative lyso-Gb3, as well as pharmacological inhibition of GLA, led to elevated levels of ASIC1a mRNA and protein in HEK cells and primary mouse cortical and hippocampal neurons. Here, GLA is linked to Fabry disease.