The observations that knockdown of disease-causing LCD-containing RBPs (i.e., TDP-43, ATXN2, hnRNP A1, hnRNP A2B1) suppresses the toxicity caused by other disease-associated proteins (i.e., VCP and DPRs) demonstrates that although disease-causing RBPs have separate functions, they are constituents of stress granules and normally maintain the material properties (i.e., assembly/disassembly rates, mobility, and viscosity) of stress granules, further strengthening the hypothesis that stress granules are dysregulated in ALS and FTD. The gene discussed is TARDBP; the disease is frontotemporal dementia.