Finally, the analysis of serine/threonine kinase (CHK2) modulation, a key component of the DNA damage response, highlighted that, in a pro-oxidant environment (50 μM and 100 μM H2O2 for 24 h), there was an increase of its phosphorylated form in SSc Hfbs (50 μM H2O2: 5.4 ± 2.1 and 100 μM H2O2: 5.5 ± 1.5, p < 0.05), independently of the presence of sildenafil (p > 0.05) (Figure 2B). The gene discussed is MARK2; the disease is systemic sclerosis.