A growing body of evidence suggests that the primary response triggered by moderate, clinically relevant doses of cancer therapeutic agents is a sustained proliferation block and not apoptosis in most human cell types (e.g., dermal fibroblasts, solid tumor-derived cells) [6,11], with activation of p53 signaling suppressing (rather than promoting) apoptosis [12,13,14]. The gene discussed is TP53; the disease is cancer.