TP73 and neoplasm: Loss-of-function, caused by the inability to bind the wild-type p53 target genes essential for tumor suppression; dominant negative effect (DNE) by forming hetero-tetramers with wild-type p53 [34], p73 or p63 [64] and the gain-of-function (GOF) propensity [65–68] which heavily depends on the context and include, cooperation with other oncogenes like HIF1a to withstand the hostile hypoxic environment, promoting cytokine secretion, angiogenesis and persistent cell cycling [69, 70], escaping cell death, immune evasion and enabling DNA damage repair and fueling nutrients [71].