These treatments primarily involve immune-checkpoint-inhibitor therapy, but recent work demonstrated that inhibiting Werner helicases in MMRd tumors may induce synthetic lethality and potentially allow for additional treatment options [78,82,83] Further supporting this notion, studies carried out in pancreatic cancer found associations between MMR signatures and antitumor immune activation, even when canonical HR or MMR genes were not germline mutated in the tumors (Table 1) [84]. The gene discussed is MRC1; the disease is familial pancreatic carcinoma.