Finally, hepatic steatosis in ALD coincided with reduced cAMP levels and increased PDE4A‐PDE4D isoform levels, both in alcohol‐fed mice and patients with ALD; Rolipram‐mediated PDE4 inhibition restored cAMP levels in the liver of these mice and attenuated lipid accumulation, underscoring the importance of regulated PDE4‐mediated cAMP signalling in lipid metabolism [20, 39]. This evidence concerns the gene PDE4A and fatty liver disease.