HIF‐1α facilitates tumor cell adaptation to the hypoxic microenvironment[36] and has been reported to activate LDHA expression by binding a hypoxia response element (HRE) within its promoter.[37] Thus, to determine whether a EBV‐miR‐BART18‐3p‐dependent increase in LDHA expression in CRC is mediated by HIF‐1α, we evaluated the mRNA expression levels of LDHA and HIF‐1α after EBV‐miR‐BART18‐3p overexpression and knockdown. This evidence concerns the gene HIF1A and neoplasm.