FASN over-expression may actively contribute to malignant-phenotype development, maintenance, and/or promotion, because its inhibition by orlistat induces cell-cycle arrest and apoptosis in a wide variety of cancer cell lines including prostate, breast, gastrointestinal, chronic lymphocytic leukemia, and others [293-296], suggesting a role for FASN in the molecular integration of a number of signalling pathways that functionally link metabolism, proliferation, and survival in malignant cells. This evidence concerns the gene FASN and B-cell chronic lymphocytic leukemia.