For example, in lung cancer, HACE1 deletion could promote KRasG12D-driven lung cancer progression by modulating the tumorigenic activation of RAC-family GTPases [29]; HACE1 could accelerate autophagic flux to inhibit tumor growth by ubiquitinating the autophagy receptor and could serve as an autophagy-related target for immunotherapeutic intervention [37]; HACE1 reduced the accumulation of HIF1α during cellular hypoxia by decreasing the stability of the protein, thus achieving the purpose of inhibiting tumor growth. This evidence concerns the gene HACE1 and lung carcinoma.