The experimental rationale for the use of MNCs in stroke therapy includes a number of mechanisms of action, such as the modulation of local and systemic inflammation, promotion of angiogenesis and endogenous neurogenesis, differentiation into cell types that facilitate cellular repair processes, and secretion of neurotrophic factors from the acute phase to the chronic phase after stroke [10,11,12] (Figure 1) (Table 1). This evidence concerns the gene NTF3 and stroke disorder.