In terms of the enhanced mitochondrial functions by overexpression of NDUFB3, combining our data with the report can provide a hypothetic explanation that in the tumor microenvironment or upon endogenous stimuli, NDUFB3 methylated by METTL9 actively enhances complex I activity by upregulating MT-ND5 subunits, thus increasing ATP levels, enhancing mitoROS generation, and improving mitochondrial function. Here, METTL9 is linked to neoplasm.