For example, overexpression of ALS-causing genes (e.g., TDP-43, FUS, and superoxide dismutase type 1 (SOD1)) enhances the recruitment of Ago2 into stress granules by facilitating the interaction between Ago2 and poly(rC)-binding protein 1 (PCBP1, a component of stress granules) [103]. Here, PCBP1 is linked to amyotrophic lateral sclerosis.