p53 mutations have been widely linked to increased tumor oncogenesis through both gain-of-function interactions, for example by promoting HIF1A-regulated angiogenic genes (Amelio et al., 2018), and loss-of-function mutations, for example by abrogating wild-type p53 repression of FBL expression, culminating in increased ribosome biogenesis (Marcel et al., 2013). The gene discussed is TP53; the disease is neoplasm.