The latter point appears critical as many synaptogenic cues overlap with angiogenic signals,27 and as TSP1/2 knockout mice as a model for long-term/lifelong complete blockade show deficits in recovery after stroke.28 In addition, as recovery-enhancing drug treatments in the clinical scenario would be applied in parallel to motor rehabilitation efforts, it will be interesting to investigate whether these interventions may stabilize the benefit on motor outcome, similar to what has been reported for other growth-promoting strategies.29 This evidence concerns the gene THBS1 and stroke disorder.