Secondly, we considered a cohort of genetically characterized patients with ALS, harboring no C9orf72 pathogenic large expansions and without clinically defined disorders related to immune dysfunctions, as representative of the general population for the first part of this study rather than considering uninfected controls, likely resistant to SARS-CoV-2 infection, to make the first comparisons and find the number of repeats in C9orf72 HRE at which the difference between COVID-19 patients and ALS patients was significant. The gene discussed is C9orf72; the disease is COVID-19.