Consequently, CerS6 overexpression and exogenous C16:0 ceramide impair breast cancer cell motility triggered by a non-apoptotic and pro-motile metalloprotease-cleaved CD95L.13 The soluble form of CD95L is produced at high levels in patients affected with TNBC and triggers the formation of a motility-inducing signaling complex.15 The low expression of CerS6, associated with a high production of the soluble CD95L in patients affected with TNBC, which exhibit a mesenchymal-like phenotype, may facilitate cancer progression and metastasis. This evidence concerns the gene FASLG and breast carcinoma.