In addition, Zhu et al. found that X-inactive specific transcript (XIST) regulated doxorubicin (DOX) resistance possibly through regulating the miR-124/SGK1 axis and that XIST knockdown enhanced the antitumor effect of DOX in colorectal cancer (CRC) in vivo, providing insights into developing therapeutic strategies to overcome chemoresistance in CRC patients [37]. Here, XIST is linked to colorectal carcinoma.