Activation of the internal tandem duplication of FMS-like tyrosine kinase 3 (FLT3-ITD) - an alteration frequently observed in acute myeloid leukaemia patients - also upregulates the SSP in a mechanistic target of rapamycin complex 1 (mTORC1)-ATF4-dependent manner, making these tumours sensitive to serine biosynthesis inhibition73. This evidence concerns the gene FLT3 and neoplasm.