Through RIP‐seq, we identified c‐FOS, a proto‐oncogene and core component of the AP‐1 complex, as a direct target of SF3A3‐mediated alternative splicing.[34] SF3A3 promoted the inclusion of exons 2 and 3 in c‐FOS pre‐mRNA, generating the full‐length isoform that activates the Bcl2/Bax signaling pathway, thereby enhancing tumor survival and cisplatin resistance.[23, 24, 34] Quantitatively, SF3A3 overexpression led to a 1–2‐fold increase in c‐FOS protein, a 1–2 fold increase in the Bcl2/Bax ratio, and a 2–3‐fold increase in cisplatin IC50, consistent with enhanced chemoresistance. The gene discussed is BAX; the disease is neoplasm.