MYF-01–37 was developed via structure-based docking to target the TEAD palmitoylation pocket. Split luciferase, qPCR, and Western blot assays confirmed inhibition of YAP-TEAD interaction and suppression of YAP target genes. Cell viability and apoptosis assays showed that MYF-01-37, combined with EGFR/MEK inhibitors, enhanced apoptosis and reduced dormant cancer cell survival. The gene discussed is YAP1; the disease is cancer.