Notably, GD3 was first implicated in apoptosis in lymphoid and myeloid tumor cells, where the activation of the apoptosis-inducing CD95 death receptor (Fas) induced GD3 synthesis and accumulation in the mitochondrial membrane, resulting in the disruption of mitochondrial transmembrane potential and apoptosis in a caspase-independent manner [11]. This evidence concerns the gene FAS and neoplasm.