Additionally, CCL5 and Fms-related tyrosine kinase 3 (FLT3) produced by NK cells or CCL4 produced by tumor cells could attract cDC1s into the tumor sites (Barry et al., 2018; Böttcher et al., 2018), but the activation of the WNT/ β-catenin signaling pathway and the accumulation of prostanoidprostaglandinE-2(PGE2) in TME could deduce the production of CCL4/CCL5, respectively (Spranger et al., 2017; Böttcher and Reis e Sousa, 2018; Ruiz de Galarreta et al., 2019). The gene discussed is CCL5; the disease is neoplasm.