Consistent with this data, PSAT1 and MTHFD1 silencing, and genetic or pharmacological inhibition of CDK12, specifically inhibited proliferation of TaxAC-resistant CDK12HIGH tumor cells in vitro, confirming the selective metabolic dependency on SGOC network hyperactivation of CDK12HIGH, but not CDK12LOW, TaxAC-resistant cells (Supplementary Fig. 7b). Here, CDK12 is linked to neoplasm.