The studies by He et al., Finisguerra et al., and Glodde et al., suggest c-MET inhibition could become an adjunct therapy to established immunotherapies because they demonstrate a role for c-MET in the recruitment of TANs, show that tumor derived GM-CSF can stimulate increased HGF-production by neutrophils and that HGF can promote increased expression of PD-L1 and PD-L2 on neutrophils. Here, HGF is linked to neoplasm.