MTHFD1L and lung cancer: Only PRDM16 and MTHFD1L are significantly enriched targets in miR-C2; miR-133, which is present in miR-C2, is reported to directly target and downregulate PRDM16 to regulate fat cell differentiation [36], and PRDM16 overexpression has been reported to inhibit EMT in lung cancer models [37].