Indeed, the fact that intrinsic or paclitaxel-acquired upregulation of BRCA1-IRIS induced expression and activation of NF-κB, as evidenced by increased expression and nuclear accumulation of p65 [44], could lead to, among other effects, transcription and secretion of a plethora of inflammatory cytokines, such as interleukin 6 (IL-6), interleukin 8 (IL-8), tumor necrosis factor alpha (TNF-α) and monocyte chemotactic protein 1 (MCP-1) that alter the tumor microenvironment through autocrine and paracrine loops [49]. Here, BRCA1 is linked to neoplasm.