An important aspect of these studies is that they demonstrate that loss of p53 function, whether by loss of protein expression (for example through a splice site mutation), missense mutation leading to variously loss of function only, dominant negative activity (DNA), gain of function (GOF) or through down-regulation of wild-type p53 using RNAi leads to a Warburg-type phenotype and more specifically to a loss of metabolic flexibility in SCCHN cells. The gene discussed is TP53; the disease is head and neck squamous cell carcinoma.