Tuberous sclerosis complex-associated seizures often does not respond well to general antiepileptic drugs due to the specific genetic mechanisms. The main pathogenic pathway of tuberous sclerosis complex is the excessive activation of the mTOR pathway due to abnormalities of TSC1 or TSC2 genes. Given that mTOR is a better antiepileptic target, preclinical and clinical studies on the efficacy and safety of mTOR inhibitors have been conducted over the last decade or so, which provides adequate evidence for the use of existing mTOR inhibitors. Currently, Rapamycin and its derivative Everolimus, among the first generation of mTOR inhibitors, have been used in clinical practice. This review summarises the evidence that, although there is insufficient evidence to confirm that Rapamycin and Everolimus significantly reverse cortical nodules in tuberous sclerosis complex, there is sufficient evidence to confirm that Rapamycin and Everolimus reduce the frequency of tuberous sclerosis complex-associated seizures and that mild-moderate adverse events are more often seen. In addition, Rapamycin and Everolimus still have limitations such as rare serious adverse events and easily recurrent seizures after withdrawal. Some of the new mTOR inhibitors currently under investigation may have efficacy and safety profiles that are not inferior to those of Rapamycin and Everolimus