Recently, Bates and colleagues6have invoked the concept of percolation, in which isolated lesions of fibrosis may, with progressive stretching, reach a critical density, at which they form an unbroken pathway extending from one boundary of the lung to the other. Thus, a decline in lung function may go undetected until fibrotic zones reached a percolation threshold, beyond which there is a sudden detectable change in lung elasticity. Indeed, unexpected rapid deterioration requiring assisted ventilation in patients with mild respiratory dysfunction, as reported in 94 patients with ILD by Fernández-Pérez and colleagues in this issue of CHEST (see page 1113),7 is in keeping with the percolation concept. Moreover, assisted ventilation could contribute to a further decline in respiratory function and reduce the chances of weaning individuals with marginal lung function off the respirator. Taking this concept further, the percolation threshold could conceivably be attained sooner in ventilated patients with a heterogeneous/patchy distribution of fibrosis, as in IPF, than in those with a more homogeneous/uniform distribution of inflammation, as in NSIP. Thus, the conditions of the patients in the former group would be expected to deteriorate faster than those with NSIP while receiving ventilatory support.