Another possibility, and one proposed by a recent study showing no exacerbation of the HD phenotype in the R6/2 mice that were also heterozygous for the gene encoding GLT-1 (ref. 46), is that ceftriaxone's beneficial effect may be independent of GLT-1 expression and rather arise from its known effect on various cell-survival transcription factors47, 48. This evidence concerns the gene SLC1A2 and Huntington disease.