Thus, both SLC4A10 and SLC9A1 seem likely to contribute to the regulation of pHi at GABAergic nerve endings and, notably, biallelic variants in SLC9A1 have been linked to a syndromic neurological disorder.57 Furthermore, control of pHi at glutamatergic presynapses is mediated by the combination of SLC9A111 and SLC4A8,58 another Na+-dependent HCO3− transporter closely related to SLC4A10. Here, SLC4A10 is linked to nervous system disorder.