Spinal Muscular Atrophy (SMA) is a genetic disorder resulting from the deletion or mutation of the SMN1 gene (Survival Motor Neuron 1). The reduction in SMN protein levels leads to the degeneration of motor neurons in the spinal cord, giving rise to typical clinical manifestations of the disease, such as muscular weakness and atrophy. At the cellular level, SMN is part of a macromolecular machinery referred to the SMN complex, comprising various proteins, including Gemin3. Among other functions, Gemin3 regulates the intracellular survival signaling pathway NF-κB. In the context of SMA disease, neuronal survival pathways NF-κB and PI3K/Akt, are altered. Currently, the precise roles of Gemin3 and these pathways in the molecular pathology of SMA remain unknown. In this study, we analyzed the association between Gemin3 levels, and SMN and IKKβ proteins in cultured mouse spinal cord motoneurons. Additionally, the impact of SMN protein overexpression on PI3K/Akt pathway has been investigated in human differentiated motoneurons of SMA type II. Our results suggest that the reduction of endogenous Gemin3 levels decreases SMN and IKKβ protein levels in mouse motoneurons, and SMN overexpression increases Akt levels in human motoneurons under SMA conditions. To draw conclusive findings, further studies are warranted to confirm that Akt phosphorylation increases upon SMN overexpression in SMA type II cells.