The finding that the interaction between p16INK4a and CDK4 under hypoxic conditions is reduced in the presence of hYSK1 suggests that hYSK1 impairs the p16INK4a-mediated decrease in CDK4 activity and hence, promotes the growth of hypoxic tumor cells by sequestering p16INK4a in the cytoplasm through protein-protein interaction. Here, CDKN2A is linked to neoplasm.