Taking into account the design of the study that precludes an effect through neuroprotection, the absence of an anti-inflammatory effect, and the possibility of an effect on IL-1β signaling, combined with the scientific literature regarding p38 MAPK-mediated deleterious effects of IL-1β on synaptic plasticity [21, 25], the results herein imply a model in which IL-1β would limit functional recovery after stroke via p38α-mediated impairment of neural and synaptic plasticity. The gene discussed is IL1B; the disease is Stroke.