Exposure of thymic carcinoma cells to HSP90 inhibitors led to cell cycle arrest and apoptosis, and blocked invasiveness, through the downregulation of HSP90 oncogenic clients, including insulin-like growth factor 1 receptor (IGF-1R), a transmembrane tyrosine kinase receptor frequently overexpressed in thymic carcinomas, CDK4, and PIK3/ Akt [32]. This evidence concerns the gene AKT1 and thymic carcinoma.