Nevertheless, it was shown recently that Staphylococcus aureus infection in Ripk3- versus Mlkl-deficient animals has opposing outcomes: Mlkl deficiency led to a delayed clearance of the bacterium, increased inflammation, and a worse outcome, whereas Ripk3 deficiency led to an improved bacterial clearance and reduced inflammation (Kitur et al., 2016), showing that the loss of Ripk3 is not equivalent to the loss of Mlkl and/or necroptosis and verifying that signaling is usually far more complex. This evidence concerns the gene MLKL and staphylococcus aureus infection.