In fact, an enzymatically inactive mutant of hPEPD, i.e., hPEPD-G278D (change from glycine to aspartic acid at position 278), was significantly more effective than hPEPD in inhibiting ErbB2-overexpressing tumors in mice, and hPEPD, but not hPEPD-G278D, stimulated prosurvival hypoxia inducible factor 1α in the tumor tissues [14]. Here, ERBB2 is linked to neoplasm.