In terms of mechanism, HDAC7 could interact with β-catenin and enhance its nucleus translocation via decreasing β-catenin acetylation level at Lys49 and phosphorylation level at Ser45 to promote fibroblast growth factor 18 expression which induced the malignant biological behaviors of NSCLC, and the HDAC7 expression could be further stabilized by USP10. This evidence concerns the gene FGF18 and non-small cell lung carcinoma.