Preclinical data show that H4R activation using the H4R agonist 4-methylhistamine not only blocked cell cycle, proliferation, and invasion of ESCC cells, but also reduced TE-2 tumor xenografts and increased the survival of tumor-bearing mice (Table 1), which suggests that H4R could be a target for ESCC treatment (He et al., 2018). Here, HRH4 is linked to neoplasm.