In a model of ventilator-induced acute lung injury (VILI), mice subjected to mechanical ventilation at high tidal volume (25 mL/kg), RIPK3 deficiency but not MLKL deficiency conferred resistance from lung inflammation and injury than their WT mice, suggesting that RIPK3-induced necroptosis is a crucial mechanism to augment inflammation and lung tissue injury [106]. This evidence concerns the gene MLKL and injury.