In melanoma, Deng et al. [135] successfully employed GCS antisense to inhibit tumor formation in an in vivo model, with a focus on ganglioside GM3 synthesis, a downstream product formed from lactosylceramide (LacCer), and work in multidrug-resistant MCF-7/AdrR (Adriamycin-resistant) cells (now termed NCI/ADR-RES cells) demonstrated elevated levels of GlcCer, LacCer, and gangliosides [9], compared with parental, drug-sensitive counterparts. This evidence concerns the gene UGCG and melanoma.