While CCL5 is generally a chemoattractant to recruit immune cells, it has been implicated in ovarian cancer resistance through activation of pathways in cells directly, either through local secretion that causes STAT2 and PI3K/Akt activation44 or through activation subsequent to BRCA1 inactivation which can lead to STING activation to promote inflammation45. This evidence concerns the gene STAT2 and ovarian carcinoma.