In TP53-wild-type NSCLC, selinexor promotes nuclear retention and stabilization of p53, leading to transcriptional activation of pro-apoptotic genes such as PUMA, BAX, NOXA, and CDKN1A (p21), thereby restoring chemosensitivity and potentiating the efficacy of standard cytotoxic therapies. Here, CDKN1A is linked to non-small cell lung carcinoma.