To establish whether the cGAS/STING pathway is responsible for neuroinflammation in response to aberrant TDP-43 in vivo, we used the well-described murine model of ALS with human TDP-43 (p.A315T) overexpression in mice (referred to as Prp-TDP-43Tg/+) (Wegorzewska et al., 2009). Here, PRNP is linked to amyotrophic lateral sclerosis.