The following are possible reasons for the contradiction: (i) different cancers have distinctive tumor microenvironments; (ii) our study was performed ex vivo which may not reflect the effect of multiple factors in vivo, including the ligation of PD-1 and PD-1 ligands and IL-33 activation by ILC2s; and (iii) we speculated that PD-1 upregulation represented activation in the early stage of ILC2s but functioned as an inhibitory factor in later stages, similar to cytotoxic T cells (36). This evidence concerns the gene PDCD1 and cancer.