Although it is still unclear whether PLS3 expression is regulated by cis- or trans-acting factors, it would appear that high PLS3 expression serves to rescue the spinal muscular atrophy patient from the detrimental effects of SMN1 deletion by promoting axonogenesis through elevation of the level of F-actin (Oprea et al. 2008) and ultimately by improving neuromuscular transmission (Ackermann et al. 2013). This evidence concerns the gene SMN1 and proximal spinal muscular atrophy.