This hypothesis is corroborated by the absence ofmodulation of Ucp1/UCP1 gene/protein expression in SOD1-G93A BAT(Fig. 1K–L).To deeper investigate the overall alterations in the molecular environmentof BAT in the ALS context, we performed 2D-Enrichment analysis between totalproteome and transcriptome in the Perseus platform [43]. This evidence concerns the gene UCP1 and amyotrophic lateral sclerosis.