AEA can also be produced through the hydrolysis of N-acyl-phosphatidylethanolamines (NAPEs) by the enzyme NAPEPLD—that was downregulated in the blood of TD patients aged 5–9 [66]—or by the combined action of the enzymes ABHD4 (downregulated in the blood of TD patients aged 13–16) and GDE1 (of which the expression in blood was negatively correlated with TD severity) [66,67]. The gene discussed is ABHD4; the disease is thanatophoric dysplasia.