Since CTSD has previously been proposed to inhibit tumor cells quiescence by activation of mammalian target of rapamycin complex 1 (mTORC1) signaling [28], we tested the effect of extracellularly applied CTSD on signaling pathways in MDA-MB-231 cells and found that it induced phosphorylation of AKT and mTOR, an effect which was blocked by coapplication of PEAR1 (Suppl. The gene discussed is MTOR; the disease is neoplasm.