Our previous studies indicated that A2AR is a potential drug target for ALS because treatment with an A2AR agonist (JMF1907; a T1-11 analog) prevents reactive oxygen species (ROS)-induced TDP-43 mislocalization in a motor neuron cell line (NSC34) and delays motor impairment in a TDP-43 transgenic ALS mouse model. This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.