CerS6 preferentially produces C16:0 dihydroceramide, which is further metabolized to C16:0 ceramide and more complex C16:0 SLs, such as C16:0 sphingomyelin and glycosphingolipids, which are both enriched in the plasma membrane microdomains.2 Our study pinpoints that the downregulation of CerS6 in TNBC is associated with an increased plasma membrane fluidity, which favors breast cancer cell motility. This evidence concerns the gene CERS6 and breast carcinoma.