However, starting from early studies investigating the role of PHGDH in tumorigenesis, it emerged that the supplementation of exogenous Ser, or a cell-permeable methyl-serine-ester, does not abolish detrimental effects of the PHGDH knockdown on tumor cells, arguing the contribution of broader Ser-independent effects for PHGDH [3]. This evidence concerns the gene PHGDH and neoplasm.