Shortly after, we found that its antitumor action—especially in hematological cancer cells—was due to the reorganization of membrane raft domains [180,181,184,186,187,188,189,190,191,192,193], leading for the first time to the activation of the Fas/CD95 death receptor from within the cell, independently of its ligand FasL/CD95L, through its recruitment in membrane raft scaffolds [184,186]. This evidence concerns the gene FASLG and hematopoietic and lymphoid cell neoplasm.