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. Here, HIF1A is linked to neoplasm.