Our finding that simultaneous inhibition of the lysosome and endosomal trafficking inhibits the proliferation of TSC2-deficient cells provides a novel potential therapeutic avenue for the treatment of TSC and other diseases associated with mTORC1 hyperactivation, including lymphangioleiomyomatosis (LAM) and the majority of human malignancies. This evidence concerns the gene TSC2 and lymphangioleiomyomatosis.