Mechanistically, we found that Ces1d/CES1 promotes CRC cell survival via at least two cell-autonomous mechanisms: 1) It increases TAG and CE breakdown to mobilize endogenous FFAs and produce ATP by FAO during starvation, thus enabling CRC cells to meet their energy demand; 2) it prevents the toxic buildup of neutral lipids that results in ROS production and phospholipid peroxidation, triggering apoptosis and ferroptosis16 (Figure 1). This evidence concerns the gene CES1 and colorectal carcinoma.