HDAC3, one of chidamide’s targets, has been implicated in chemoresistance in various malignancies: it is essential for Kras-mutant lung cancer progression by co-regulating transcription with NKX2-1 and promoting FGFR1 expression, with its inhibition restoring trametinib sensitivity [30]. This evidence concerns the gene FGFR1 and lung carcinoma.