The transient overexpression of HDAC5 resulted in increased proliferation and augmented migration and invasion in GC cells (SGC-7901 and HGC-27 cells) compared with the blank control; the combination of the transient overexpression of HDAC5 and p16INK4a abolished the promoting effect of HDAC5 on GC cell proliferation, migration and invasion, while the combination of the transient knockdown of HDAC5 and p16INK4a markedly reversed the inhibitory effect of silencing HDAC5 on GC cell proliferation (Fig. 7A and Suppl. Here, HDAC5 is linked to gastric cancer.