Background and Aims The nuclear transport system is intrinsically linked to tumor-relevant signaling cascades and selective inhibitors of nuclear export represent a promising approach for cancer treatment. The exportin-1 (XPO-1) inhibitor selinexor is already approved for treating hematological neoplasms, whereas its efficacy in solid tumors including liver cancer is poorly understood. In this study we aim to identify candidates potentially involved in selinexor response/resistance.