MiR-99a and miR-100 were highly expressed in ACC and they could contribute to malignant growth and progression of ACC by regulating IGF-mechanistic target of rapamycin kinase (mTOR) signaling, thus promoting the cell cycle.[112] Pharmacological inhibition of mTOR signaling using everolimus greatly decreased tumor cell growth in vivo and in vitro. The gene discussed is MTOR; the disease is neoplasm.