Introduction: Tuberous sclerosis complex (TSC) is characterized by cortical tubers, with epilepsy occurring in approximately 80-85% of patients. Although the ""second-hit"" hypothesis of biallelic TSC1/TSC2 inactivation has been proposed to explain tuber formation, the complete genetic architecture remains unclear. Objectives: To investigate somatic mosaic variants in TSC cortical tubers using brain tissue obtained from stereoelectroencephalography (SEEG) electrodes. Methods: We prospectively enrolled 8 patients with drug-resistant epilepsy and TSC who underwent SEEG-guided radiofrequency thermocoagulation. Genomic DNA was extracted from electrode-adhering brain tissue and subjected to wholeexome sequencing at a mean depth of 1000×, with candidate variants validated by amplicon sequencing. Results: Among the 8 patients (5 males; 2 with germline TSC1 mutations and 6 with TSC2 mutations), somatic mosaic variants in mTOR pathway-related genes were identified in 2 patients. Patient 2 harbored a PTPN11 missense variant (p.Asp61His, VAF 8.1%) with a germline TSC1 nonsense mutation. Patient 3 harbored a MAPK1 missense variant (p.Pro247Leu, VAF 3.7%) with a germline TSC2 frameshift mutation. Both patients presented with focal cortical dysplasia type IIb-like lesions with transmantle sign. Notably , no classic TSC1/TSC2 second-hit mutations were detected. Functional predictions indicated both variants are gain-of-function mutations enhancing RAS-MAPK signaling, increasing inhibitory phosphorylation of the TSC complex through a ""dual-hit"" mechanism. Conclusions: We propose a third pathogenic mechanism for TSC cortical tuber formation characterized by low-level somatic mosaicism in mTOR pathway regulators rather than classic TSC1/TSC2 second hits. This "pathway convergence” model provides a new framework for understanding phenotypic heterogeneity in TSC.