Compound 6 was associated with G0/G1 phase arrest, reflecting disruption of early cell cycle progression.48 In contrast, FW-04-806 induced G2/M arrest, whereas compound 11g caused S-phase accumulation in A549 lung cancer cells, indicating inhibition of DNA synthesis or replication stress.50,73 Additionally, DDO-5936 induced G1-phase arrest through the downregulation of CDK4, a known client of the Hsp90–Cdc37 complex.54 Together, these mechanisms result in the irreversible loss of proliferative capacity, offering a dual-hit strategy of inducing cell death while halting tumor growth. Here, CDK4 is linked to lung cancer.