Several biological explanations have been offered for the lack of correlation between FLT and Ki-67: the absence of cell cycle-specific regulation of thymidine kinase 1 [30]; the heterogeneity of Ki-67 expression within tumor samples; variations in cellular ATP levels; Ki-67 expression being related to cellular proliferation via the salvage pathway as well as the de novo pathway, while FLT uptake is likely only related via the salvage pathway [31]. Here, MKI67 is linked to neoplasm.