In non-small cell lung cancer (NSCLC) models, pharmacodynamic consistency was observed between USP1 inhibition and biomarker modulation, specifically the accumulation of monoubiquitinated PCNA, which was correlated with clonogenic suppression.588 The covalent USP2 inhibitor ML364 shows biochemical potency (IC50 of 1.1 μM), with on-target effects, including a reduced Cyclin D1 half-life, G1-phase arrest, and selective antiproliferation. Here, USP2 is linked to non-small cell lung carcinoma.