Tan, B. et al. demonstrated that Rspo-LGR4 axis functioned as a novel pathway aggravating M2-like macrophage polarization through noncanonical Erk/Stat3 signaling by recruiting IQGAP1 and MEK1/2, thus maintaining protumoral TAMs, promoting tumor progression and enhancing the resistance of Lewis lung carcinoma (LLC) cells to anti-PD1 treatment. This evidence concerns the gene RSPO1 and neoplasm.