Given the importance of GCN5 HAT complexes for Myc-dependent transcription and transformation in human cells and the synthetic lethality of GCN5 deletion and CG-1521 treatment in yeast, it is likely that the effect of GCN5 knockdown (or inhibition of the acetyl transferase activity) combined with CG-1521 administration in Myc-driven tumors will lead to the blockade of tumor progression. This evidence concerns the gene TMPRSS11D and neoplasm.