However, multiple lines of evidence point to disrupted SG function in these conditions: loss and/or gain of function by several ALS-related proteins, including FUS, TDP-43, angiogenin, C9ORF72-derived dipeptides and hGLE1, negatively affect SG integrity.43, 44, 45, 46, 47, 48 The fact that core SG proteins, such as PABP1 and eIF4G, are found accumulated in pathological inclusions in postmortem tissue49 also implies a decline of their functional pools and associated deficits in SGs formation. The gene discussed is GLE1; the disease is amyotrophic lateral sclerosis.