RAD52 overexpression was reported to correlate with hepatocarcinogenesis in TGF-α/c-myc mice [92], and its depletion or inhibition was reported to decrease cancer incidence and exert antileukemic effects in ATM-deficient mice [93] and in acute myelogenous leukemia (AML), B-cell acute lymphoblastic leukemia (B-ALL), and T-cell acute lymphoblastic leukemia xenografts with low BRCA1/2 expression [84]. Here, RAD52 is linked to cancer.