Ventilating a patient with an IPF exacerbation is a diffi cult and demanding task, and no 'cookbook' prescriptions can make the work easier for the intensivist. Th e evidence for the best ventilator strategy applying to an IPF exacerbation is extremely scarce, and the eff ect of ventilatory management on outcome has not been system atically assessed; therefore, every suggestion is based on theoretical principles and pathologic data that are characterized mainly by extended DAD [7] . Recently, Bates and colleagues [65] introduced the concept of percolation, according to which the progression of parenchymal lung disease can suddenly reach a threshold that dramatically alters the mechanical properties of the lung. IPF exacerbations that require ventilator support could be an example of crossing this percolation threshold. Under these circumstances, mechanical ventila tion could represent a second hit for the lung parenchyma, further deteriorating the mechanical properties of lung parenchyma and introducing a vicious cycle that ends in death. Mechanical ventilation with conventional volumes (8 mL/kg) in patients without lung injury can induce severe surfactant impairment, and sustained plasma cytokine production has been demonstrated in patients without ALI ventilated with conventional tidal This non-proportional fi gure denotes the incoherence of the clinical signifi cance of acute respiratory distress syndrome (ARDS), acute interstitial pneumonia (AIP), and idiopathic pulmonary fi brosis (IPF) exacerbations in which DAD, despite being the common denominator, develops upon diff erent histology substrates (UIP in IPF exacerbations, normal lungs in AIP, and normal or diseased lungs in ARDS) and, according to current defi nitions, presents at diff erent time intervals: 7 days for ARDS, 4 weeks for IPF exacerbations, and 2 months for AIP. This incoherence led also to a diff erent pharmacologic approach, which proved to be unsuccessful at least in AIP and in IPF true exacerbations. ALI, acute lung injury.