Structural analysis of the oxidized structure revealed that the oxidation of Noxa1 SH3 made it unstable with higher flexibility, which aligned with experimental investigations showing that CAP treatment caused denaturation of Noxa1 SH3 and subsequent inactivation of NOX1, leading to the inhibition of cancer cell proliferation, differentiation, growth, and tissue regeneration [198]. The gene discussed is NOX1; the disease is cancer.