This approach has not been investigated before and would potentiallysuggest a novel and unique mechanism of action (MOA) for Gal-3 inhibitors on enhancing antitumor immunity with checkpoint inhibitors.Further characterisation of this potential MOA was performed in vitro by investigating the effect of GB1211, a Gal-3 selective small molecule inhibitor currently in clinical development (16) as a combination therapy with atezolizumab in patients with advanced NSCLC (NCT05240131), on reversing Gal-3 binding to PD-1 and PD-L1 in the absence and presence of the ICIs. This evidence concerns the gene PDCD1 and non-small cell lung carcinoma.