Spinal Muscular Atrophy (SMA) is an autosomal recessive neuromuscular disease caused by the loss of the survival motor neuron (SMN1) gene in over 95% of cases. However, mutations in genes associated with the SMA chromosomal region can influence disease progression. Aim: To analyze the status of the NAIP and GTF2H2 genes in correlation with SMA. The study included 120 patients suspected for SMA of which 55 with confirmed with SMA and 65 without causative deletions, and 130 healthy, unrelated individuals. The molecular genetics methods used were multiplex PCR, PCR-RFLP and MLPA. From 120 patients, 57 were confirmed with SMA. In this group were identified in 9 patients (15%) with a homozygous deletion of exon 5 of the NAIP gene, 4 patients (7%) had a heterozygous status, and 2 (4%) had duplications. In the rest of the patients (63), in which deletions of SMN1 exon 7 were not identified, homozygous deletion of exon 5 of the NAIP gene was established in one patient (3%), 3 patients (5%) had duplications of exon 5 of the NAIP gene, and one patient had 5 copies of the NAIP gene. In the 130 healthy controls, one patient (1%) was identified with a deletion of exon 5 of the NAIP gene. None of the patients with combined deletions of SMN1 and NAIP had deletions in GTF2H2. The frequency of deletions in the NAIP gene was found to be higher in the SMA patient group compared to the control group. Thus, a significant relationship was identified, the P value being <0.00001. The significance threshold was set at p<0.05. Our investigation is the first to examine the relationship between SMN locus genes and SMA in the Moldavian population. The genetic patterning of genes associated with SMA is an important aspect in the study of molecular pathophysiology and assessment of disease prognosis, especially in the approach to gene therapies.