Amyotrophic lateral sclerosis (ALS) is characterized by progressive death of motor-neurons (MNs) by a complex interplay of multiple predisposing-factors. The discovery of miscellaneous ALS-associated mutations signifies the genotypic and phenotypic heterogeneity of ALS. Mutations in the gene for intracellular scavenging enzyme, Cu/Zn-superoxide dismutase (SOD1) are linked to MN-dysfunction in 10-20% of familial-ALS cases and 1-5% of sporadic-ALS cases. However, not every MN type displays vulnerability to ALS-causing mutation to the same extent and this selective-susceptibility of MN-subpopulations unfolds a striking opportunity to investigate the determinants of ALS-neurodegeneration. The segmental-distribution of MNs along the antero-posterior (A-P) axis is orchestrated by ranked expression of Hox genes, while the exact contribution of this A-P positional identity to the timing and extent of MN-vulnerability to ALS is not understood clearly. This project was centred on the objective to delineate any link between the A-P axial-identity of MN-columns and their selective-vulnerability to specific ALS linked mutation by examining transcriptomic changes in spinal cord samples with two distinct axial-identities (cervical and lumbar) using a publicly-accessible mutant-SOD1 mice (rodent model of SOD1-linked ALS) dataset. Additionally, Gene Ontology (GO) enrichment analysis was performed on the differentially expressed (DE) genes in cervical and lumbar spinal-cords to portray a comparison between the vulnerability of these axially definite MN-subgroups, which revealed an augmented protective inflammatory-response in the mutant-SOD1 cervical spinal-cords. An improved understanding of the influence of A-P axial-identity of MNs on the intricate ALS-linked pathological processes by further experiments may be harnessed for unlocking the way to discover potentially curative therapeutic applications for this deadly neuromuscular disease.