Substrate-selective mTORC1 regulation and gene dosage–dependent tissue divergence in Birt–Hogg–Dubé syndrome
An integrated pathogenic framework is described that drives renal tumorigenesis via constitutive MiT/TFE nuclear accumulation and metabolic reprogramming and highlights novel therapeutic vulnerabilities targeting MiT/TFE factors and kinase rewiring, providing a rationale for organ-specific precision medicine in BHD.