We show here that an optimized version of this peptide (VGCARRYCS, disulfide-bridged, called “G4”) can bind and block the active site of CD13 with high affinity and selectivity, but not after fusion to TNF or after coupling to other bulky compounds; nevertheless, we also show that the G4-TNF fusion protein can still target tumor lesions, when administered to tumor-bearing mice, through a CD13-dependent mechanism. The gene discussed is ANPEP; the disease is neoplasm.