To explore the mechanisms underlying the effects of this combination, we investigated a part of the DNA damage repair pathway related to DNA double-strand breaks (DSBs) because MEK inhibition might induce dependence on DSB repair in KRAS-mutant cancer cells, and SUMOylation inhibition could block Rad51 function, which plays a critical role in DSB repair [26–29]. The gene discussed is KRAS; the disease is cancer.