Spinal Muscular Atrophy (SMA) is a neurodegenerative disease that occurs in 1 of every 6,000 births, and is caused by low levels of the SMN protein. SMA patients have inherited deletions or mutations of SMN1, one of two genes encoding SMN. SMN2 contains a translationally silent single nucleotide switch that causes mis-splicing of its transcript, rendering the protein non-functional thus unable to compensate for the loss of SMN1. Current efforts to combat SMA revolve around increasing the stability or altering the splicing of SMN2. Researchers at Nationwide Children’s Hospital have developed a novel method for modulating SMN2 splicing in a therapeutic context by inducing the heat shock response. This novel splicing-corrective treatment is capable of increasing protein levels of SMN in vitro and is being further developed for use in murine models of SMA.