Meanwhile, upon the overexpression of Myo1b, the young HUVECs tended to accelerate the senescence evaluated by the augmented number of SA-β-gal positive cells (Figure 2(b)) and the occurrence of endothelial dysfunctions, e.g., the impaired NO production (DAF-2DA) and enhanced intracellular superoxide production (Figure 2(c)). The gene discussed is MYO1B; the disease is endothelial dysfunction.