When the concentration of ANXA114‐26 is higher, the binding rate to FPR is higher, which blocks the binding of ANXA1 secreted by tumor cells or TME‐related cells to FPR, so with the increase of the concentration of ANXA114‐26, the binding rate of ANXA1 to FPR decreases, and the apoptosis of ovarian cancer cells increases, and drug resistance decreases. This evidence concerns the gene FPR1 and ovarian carcinoma.