Dysfelinopathy is a rare type of muscular dystrophy that is caused by the improper function of dysferlin. Its primary function is to patch and repair tears in the muscle cell membrane. When there is a tear, the dysferlin will travel to the membrane to repair it.  Dysferlinopathy occurs when there are mutations within the dysferlin gene that cause it to misfold in the ER. This misfolding inhibits its ability to repair the muscle cell membrane, leading to muscle weakness and eventually the inability to use the muscle completely. The first project was looking at the differentiation between the wild type and DYSF mutants. The differentiation between the DYSF mutants will allow us to predict what kind of effects some drugs can have on the disease. It was revealed that the DYSF mutants differentiated faster than the wild-type myoblasts. The second project was using the drug TUDCA to see if it is able to restore dysferlin protein to the membrane. TUDCA is a drug that is already FDA-approved for other diseases and has been shown to reduce endoplasmic reticulum stress. There are currently no drug treatment options available for patients with this disease. If TUDCA were revealed to be working, it would provide a viable drug option for the patients. During these studies, it was revealed that TUDCA increases dysferlin protein at the membrane, but the results are not yet statistically significant, suggesting that more research is needed, especially to determine the optimal TUDCA concentration.