Through in vitro experiments on astrocytic and neuronal cells and analysis of ALS brain tissues, Manghera and colleagues found that TDP-43 facilitates HERV-K reverse transcriptase protein deposition in human neurons, and that human astrocytes and neurons have cell-type specific differences in their ability to express and clear HERV-K reverse transcriptase proteins during inflammation and proteasome inhibition; astrocytes, but not neurons, cleared excess HERV-K proteins through stress granule formation and autophagy [77]. Here, TARDBP is linked to amyotrophic lateral sclerosis.