Silencing XPNPEP2 promoted a notable reduction in the steady-state level of SLC25A6 by SIAH1-mediated proteasomal degradation, resulting in a reduction in MAMs, fragmentation of mitochondria, and collapse of mitochondrial function, which was concordant with recent observations that mitochondrial dysfunction and suppression of MAM formation led to inhibition of angiogenesis and tumor vascularization (Herkenne et al., 2020; Wang et al., 2021; Ma et al., 2023; Laplace and Bonneau, 2024). The gene discussed is SLC25A6; the disease is neoplasm.