As for the lack of effect of RIPK3 deletion on the ALS-like motor phenotype, at least in female mice and on neuropathology in both sexes, we cannot exclude that the constitutive ablation of RIPK3 was mitigated by unknown molecular compensation that was stronger in female and sufficient to mask signs of neurodegeneration in both sexes. Here, RIPK3 is linked to amyotrophic lateral sclerosis.