MTOR and endometriosis: In endometriosis, hyperestrogenic conditions and chronic inflammation cause sustained mTOR activation, NF-κB positive feedback, and constitutive stimulation of the PI3K/AKT/mTOR and MAPK/ERK pathways, resulting in autophagy suppression, abnormal proliferation, lesion maintenance, and infertility [126,127,128,129,130,131,132,133].