Referring thereafter directly to the steps numbered in Figure 7, these events include (1) the enhanced cell synthesis and levels of coenzyme A (PPARα) along with (2) increased mitochondrial acyl-CoA synthetase (ACS) activities (PPARα) favours (3) the formation of long-chain fatty acyl-CoAs for which the accumulation(4) is strengthened by deficiency of their removal via glycerol esterification (deficient glycerol 3P dehydrogenase in cancer cells), (5) and is known to inhibit hexokinase forms (metabolic regulation). The gene discussed is PPARA; the disease is cancer.