Previously, it has been reported that the angiotensin-converting enzyme (ACE)-C domain overexpression in macrophages would result in the transformation of macrophages toward the M1 phenotype in tumor microenvironment, accompanied by enhanced activation of NF-κB and signal transducer and activator of transcription 1 (STAT1) and attenuated activation of STAT3/6 [28]. Here, ACE is linked to neoplasm.