We also examined the relative contribution of mTORC1 and mTORC2 signaling in primary human dermal fibroblasts (pHDFs), hepatic stellate cells (HSCs), and cancer-associated fibroblasts (CAFs) derived from patients with lung adenocarcinoma by CRISPR-Cas9 gene editing to disrupt mTORC1 (RPTOR) and mTORC2 (RICTOR) signaling. The gene discussed is RICTOR; the disease is lung adenocarcinoma.