To gain insights into the early detrimental actions of LPA2 in ALS, we focused our experiments on SOD1G93A mice at 16 weeks of age, when neurological outcomes were markedly enhanced in ALS mice lacking lpar2. Since LPA mediates gliosis and we recently reported that microglial cells become cytotoxic upon LPA2 stimulation (López-Serrano et al., 2019), we first evaluated whether LPA2 signaling contributed to microgliosis and astrogliosis in the lumbar spinal cord of SOD1G93A mice. The gene discussed is LPAR2; the disease is amyotrophic lateral sclerosis.