Furthermore, we evaluated the ability for these SINE molecules to impact cell proliferation using in vitro models expressing wildtype or E571K-mutated XPO1. First, employing a HEK293 tumor cell model we have previously designed for heterozygous expression of XPO1-E571K in the endogenous locus via CRISPR-based gene editing techniques [50], we observed a similar, dose-dependent, inhibitory response upon 48 h of exposure to SINE molecules KPT-185, KPT-330 or KPT-8602 between both wt and XPO1-E571K expressing cells (Fig. 4c). The gene discussed is XPO1; the disease is neoplasm.