Next, we reasoned that most m6A-modified ALS risk genes could potentially contribute to the observed ALS-like pathologies upon m6A impairment in the ChAT-Cre; Mettl14floxed mice, so we probed the consequence of hypo-m6A for MNs by performing 10x Genomics single-nuclei multimodal profiling of ATAC/RNA (snATAC/RNAseq) on Ctrl (ChAT-Cre; Mettl14f/+) and ChAT-Cre; Mettl14floxed mice, allowing us to assess chromatin accessibility and gene dysregulation in a range of MN subtypes simultaneously (Fig. 6a, b). This evidence concerns the gene CHAT and amyotrophic lateral sclerosis.