YAP enters the mTOR pathway to promote tuberous sclerosis complex.

Mutations in tuberous sclerosis complex 1 (TSC1) or TSC2 predispose to angiomyolipomas and lymphangioleiomyomatosis in a mTOR-dependent manner. In these mesenchymal lesions, mTOR suppresses macroautophagy-mediated lysosomal degradation of YAP, which is a transcriptional coactivator of Hippo pathway and is required for the tumorigenesis of TSC. Therapeutic applications for TSC and other diseases with dysregulated mTOR activity can be envisaged.