Knockdown of CERS6 in colon adenocarcinoma cells caused a decrease in C16-Cer and protected the cells against tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)16, whereas C16-Cer generated by CERS6 in human head and neck squamous cell carcinoma (HNSCC) cells increased tumor development and growth17, suggesting an anti-apoptotic role of CERS6 in tumor cells. Here, CERS6 is linked to neoplasm.