Abstract
Summary Signalling proteins, which are often mutated in cancer, change transcription patterns. Many more signalling proteins are affected in cancer than transcription factors, electing transcription factors as cogent targets. One or more latent cytoplasmic transcription factors (such as STATs, NF-κB, β-catenin and Notch intracellular domain (NICD)) have increased activity in most human cancers, and in many cases prevent apoptosis of cancer cells. Necessary physical interaction among transcription factors and cofactors in the nucleus affords selective sites of potential drug action. Should pharmacology of transcription-factor inhibition be the wave of the future? It might be difficult, but it should not be impossible.