Since IL-2 regulates p21 in cervical cancer cells, one possible explanation for this increase in cell viability is that IL-2 stimulates activation of the DNA repair pathway, in which p21 is an important molecule; p21 binds to and inhibits CDK, preventing the phosphorylation of BRCA, which aids in binding of the nucleoprotein RAD51 to ssDNA, thus promoting DNA repair [57]. The gene discussed is CDKN1A; the disease is cervical cancer.