In their study, by devising a dual perturbation library designed to target both mutated tumor suppressor genes and immune resistance genes, they revealed that the simultaneous KO of Jak1/Jak2 and tumor suppressor genes such as Trp53 resulted in an increased resistance to OT-I CD8+ T cells during combinatorial antineoplastic drug resistance experiment (CADRE) screening, which suggests the existence of intricate gene interaction.64 The gene discussed is JAK2; the disease is neoplasm.