GPRASP1 and breast cancer: 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.