PRDM16 and neoplasm: Control of tumor vascularization was reflected in depletion of mutations in PRDM16, which inhibits angiogenesis by suppressing the expression of a HIF target semaphorin 5B (Kundu et al., 2020), and in NCO1A, a transcriptional coactivator that upregulates the expression of the VEGFα pro-angiogenic factor (Qin et al., 2015).