Next, to address whether improvements in kinesin-1/KIF5A distribution could underlie JNK1 overexpression-induced process formation, we performed SR-SIM analysis of KIF5A/GFP co-labelling in GFP-transfected (GFP + ) SOD1 ALS astrocytes and in JNK-GFP-expressing (JNK-GFP+) and non-JNK-GFP-expressing cells (JNK-GFP-) in JNK-GFP-transfected ALS astrocyte cultures. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.