SOD1 and amyotrophic lateral sclerosis: In general, the mouse-human correspondence was improved in SOD1-G93A mice having a more advanced phenotype (symptomatic or endstage) (Figure 6), with increased expression of ALS-increased DEGs associated with inflammation (F3, C3AR1, CYBB) and decreased expression of ALS-decreased DEGs associated with neuron generation (CAMK1D, HECW1, SLITRK4) (Supplementary Figure S26).