Although the prognosis of CF has remarkably improved with the introduction of modulators to target the specific mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene [3], there has been limited progress in defining the underlying mechanisms involved in altered EFA metabolic pathways [4,5] and the anti-inflammatory effect of the dietary modulation of EFA deficiency [6,7]. Here, CFTR is linked to cystic fibrosis.