We hypothesized that OGT activity is remodeled in response to CDK9 inhibitor treatment because combined inhibition of OGT and CDK9 is toxic to prostate cancer cells [23], OGT activity is remodeled in response to stress [25, 31] and OGT-dependent glycosylation alters protein function [24, 34]. The gene discussed is CDK9; the disease is Familial prostate cancer.