This study investigated the potential of the drug Ataluren to treat Cowden syndrome caused by nonsense mutations in the PTEN gene. The researchers grew lymphoblast cell lines from a patient with Cowden syndrome and normal control cells. They treated the cells with varying concentrations of Ataluren and analyzed the levels of functional PTEN protein produced. They found that Ataluren did not increase PTEN protein levels in the patient cells, suggesting it does not induce read-through of premature stop codons for this mutation. However, more testing is needed using cell lines with different PTEN mutations to fully understand Ataluren's effectiveness.