This is further supported by evidence that knockout of the ALS risk gene CAV1 [52] in endothelial cells, whose proportion in samples assigned to this cluster was significantly higher, can reduce innate immune system signalling via activation of endothelial nitric oxide synthase (NOS3) [53]; a complex of which was observed in our enrichment analysis. Here, CAV1 is linked to amyotrophic lateral sclerosis.