However, in a recent report, when p16INK4A was expressed under the control of Tet repressor system in glioma cells on a long-term basis, it decreased the expression of Rb, suggesting that this gene therapy approach involving p16INK4A, could ultimately have led to the selection of Rb-deficient gliomas (Simon et al., 2002). This evidence concerns the gene RB1 and central nervous system cancer.