Only two studies have investigated this issue, indicating that elevated S100A4 expression in cancer cells may activate the NF-kB signaling pathway, inhibit p53 expression, and contribute to cisplatin resistance (56); Lung fibroblasts can stimulate the secretion of S100A4 in resistant OC cells via the IGF1R-α6 integrin-S100A4 pathway, resulting in its activation and enhancing the metastasis and colonization of late resistant cells (57). The gene discussed is IGF1R; the disease is cancer.