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Among them, lncEGFL7OS, located in the opposite strand of the EGFL7\/miR-126 gene, is regulated by ETS factors through a bidirectional promoter in ECs. It is enriched in highly vascularized human tissues, and upregulated in the hearts of dilated cardiomyopathy patients. LncEGFL7OS silencing impairs angiogenesis as shown by EC\/fibroblast co-culture, in vitro\/in vivo and ex vivo human choroid sprouting angiogenesis assays, while lncEGFL7OS overexpression has the opposite function. Mechanistically, lncEGFL7OS is required for MAPK and AKT pathway activation by regulating EGFL7\/miR-126 expression. MAX protein was identified as a lncEGFL7OS-interacting protein that functions to regulate histone acetylation in the EGFL7\/miR-126 promoter\/enhancer. CRISPR-mediated targeting of EGLF7\/miR-126\/lncEGFL7OS locus inhibits angiogenesis, inciting therapeutic potential of targeting this locus. 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