Given that FGFR2-IIIc is associated with aggressive tumor behavior and is not effectively targeted by current FGFR2-IIIb-selective therapies, a combinatorial approach targeting both FGFR2 splicing isoforms and the upstream miR-23a-ESRP1 axis may provide synergistic benefits, notably overcome isoform-driven resistance. Here, ESRP1 is linked to neoplasm.