In silico binding analyses, supported by SPR and ELISA assays, identified pGSN as a key binding partner of DCLK1 isoform 4, with a strong affinity (KD ~ 100 nM) indicative of a critical role in pro-tumorigenic signaling.20,21 Notably, D-peptide 1 enhances pGSN binding, implying allosteric modulation that may alter downstream signaling related to tumor growth and stemness, while its weak interaction with FGF19 underscores the selective nature of these PPIs. Here, DCLK1 is linked to neoplasm.