However, in pathological contexts such as amyotrophic lateral sclerosis (ALS), FABP7 upregulation promotes NF-κB-driven pro-inflammatory signaling and astrocytic neurotoxicity, while its silencing reduces motor-neuron toxicity, underscoring its dual and context-dependent nature [150]. This evidence concerns the gene NFKB1 and amyotrophic lateral sclerosis.