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. The gene discussed is TUBB6; the disease is amyotrophic lateral sclerosis.