Given the prominent role of neuroinflammation and peripheral inflammation in ALS pathology progression (Appel et al., 2021; Beland et al., 2020; McCombe et al., 2020), we hypothesize that lymphatic structure and function are compromised in the most widely used animal model of ALS, the SOD1-G93A mouse (Gurney et al., 1994). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.