To assess the impact of CTXD14SkM-EVs treatment on NF-κB signaling in the TA muscle of SOD1G93A mice, we performed Western blot analysis to quantify the expression of total NF-κB, the active phosphorylated format of NF-κB (pNF-κB), and the loading controls GAPDH and β-actin across three experimental groups: wild-type (WT) mice, PBS-treated ALS mice, and CTXD14SkM-EV-treated ALS mice. The gene discussed is GAPDH; the disease is amyotrophic lateral sclerosis.