Aberrant activation of several signaling pathways has been reported to drive paclitaxel resistance, including NF-κB, PI3K/AKT, and MAPK/ERK pathways [31, 47, 48], as demonstrated by our data showing that GASP1 knockout sensitized breast cancer cells to paclitaxel, while GASP1 overexpression decreased their response to paclitaxel. This evidence concerns the gene GPRASP1 and breast carcinoma.