We ruled out that the observed modulation was due to a secondary off-target effect of the MET-TKi, as comparable results were obtained also inhibiting the MET pathway by means of a MET blocking antibody that, wiping out MET from the cell surface, acts through a mechanism completely different from the kinase inhibition.45 Moreover, the activity of MET inhibitors occurs peculiarly in MET-amplified systems, as IFNγ stimulation of PD-L1/PD-L2 is not revoked by MET-inhibitor treatment in tumour cells that are not MET amplified and express either inactive or HGF-activated MET. Here, HGF is linked to neoplasm.