Beyond the major pathological themes of each subtype, we observe some evidence for cytoskeletal defects and altered axonal transport in ALS-Ox and ALS-TD patients through the expression of ACTA2, DYNLT3, PLS1, and TUBB6. Moderate overexpression of FOLH1 implicates glutamate excitotoxicity in ALS-Glia patients, although further consideration of transcripts and proteins associated with glutamate metabolism and signaling are needed to explore subtype specificity. This evidence concerns the gene ACTA2 and amyotrophic lateral sclerosis.