Similarly, in the condition of ALS, GLT-1 was downregulated and its levels were influenced by components like tumor necrosis factor α (TNF-α), nuclear factor kappa B (NFκB) signaling, upregulation of astrocyte elevated gene–1 (AEG-1) andthe knocking out of membralin, an important component of endoplasmic reticulum (ER) [18,19]. Here, TNF is linked to amyotrophic lateral sclerosis.