Although why IDH mutation requires intact CDKN2A/B for conferring favorable clinical outcome remains to be investigated, its anti-tumor activity seemingly depends on the integrity of tumor-suppressor genes, as depicted in Figure 2; the activity is extinct upon CDKN2A/B homozygous deletion, weakened in the presence of TP53 alteration or 1p/19q codeletion, and most potent when the tumor-suppressor genes remain intact. The gene discussed is TP53; the disease is neoplasm.