In a PDX model of ovarian cancer lacking HR gene mutations but harboring RAD51C promoter methylation, treatment with niraparib induced a significant increase in mRAD51C mRNA, associated with loss of the RAD51C promoter methylation, indicating that RAD51C methylation can be reversed by the treatment pressure of PARPi, which restored RAD51C expression, causing PARPi resistance [121]. Here, RAD51C is linked to ovarian carcinoma.