In this work, we demonstrated that downstream of oncogenic HDAC7, LGALS3-ITGB1-mediated activation of the FAK-ERK-JUN pathway played a key role in the MES transition of GBM and the formation of a TAM-dependent suppressive TME (Figure 5), suggesting that LGALS3 was a potentially effective candidate for a therapeutic strategy that has the potential to exhibit good clinical results from both tumour suppression and optimization of HDAC inhibitors. The gene discussed is JUN; the disease is glioblastoma.