Interestingly, apart from melanoma suppression, overexpression of the studied combinations of TCA enhancing enzymes (PDH‐PDP‐GDH) or the employment of a CREB inhibitor (CREBi) led to an almost complete restoration of the phospho‐protein pattern of activated TCA enzymes (data not shown), increased TCA metabolites, and resulted in a profound suppression of glycolysis (data not shown), demonstrating that fueling of the TCA cycle and not the toxicity of accumulating substrates are responsible for our observations. The gene discussed is GLUD1; the disease is melanoma.