To further characterize the regulation of Rad51 nuclear foci formation, we pre-treated cancer cells with EGFR inhibitor Erlotinib, PI3K inhibitor LY292004, or ERK inhibitor PD98095 and found that only pre-treatment with Erlotinib led to significant reduction of Rad51-positive nuclear foci (P<0.05, Figure 4D), implying that regulation of Rad51-mediated HRR depends on upstream signaling molecule(s) such as IRS1, rather than downstream ones, such as PI3K/AKT or ERK. The gene discussed is IRS1; the disease is cancer.