Whereas blockage of de novo phosphocholine (PCho) synthesis by MN58b in primary cells induces Retinoblastoma (Rb) dephosphorylation and results in reversible cell cycle arrest in G0/G1 phase, tumor cells suffer a drastic wobble in the metabolism of main membrane lipids phosphatidylcholine and sphingomyelin, resulting in a significant increase in the intracellular levels of ceramides that promotes apoptosis [22], [23]. This evidence concerns the gene RB1 and neoplasm.