Additionally, fibroblasts derived from a patient with Hutchinson–Gilford Progeria Syndrome (HGPS) were used to generate MSCs as a cell model of premature senescence.[42] The senescence states were verified by cellular senescence markers, including higher SA‐β‐gal activity, increased expression of p53, p21, p16, and reduced proliferation (Figure 1A; Figure S1A,B, Supporting Information). The gene discussed is TP53; the disease is Hutchinson-Gilford progeria syndrome.