Under hypoxic conditions, SKA3 can bind to HIF-1α by recruiting PARP1, which in turn enhances the poly ADP-ribosylation of HIF-1α, induces the USP7-mediated deubiquitination of HIF-1α, and ultimately upregulates key lipogenic enzymes to increase the level of lipid expression, which provides a source of energy to drive the malignant proliferation of tumor cells. Here, SKA3 is linked to neoplasm.