Recent studies in renal carcinoma systems have underscored the reciprocity of this mTORC1-MiT interaction in the kidney: in the setting of TSC1/2 or FLCN loss, TFEB and/or TFE3 are constitutively activated, drive renal tumorigenesis and these transcription factors are also upstream drivers of mTOR signaling19,20,29,30, indicating that the persistent co-activation of catabolic (autophagy and lysosomal biogenesis) and anabolic (mTORC1) transcriptional programs is a hallmark - albeit paradoxical - feature of many types of renal tumors. This evidence concerns the gene FLCN and renal carcinoma.