Different anti-tumor strategies have emerged that target or exploit ERAD [28], including combining salirasib (a RAS inhibitor) with eeyarestatin (an ERAD inhibitor) due to the synthetic lethality between RAS and several ERAD genes (SEL1L, Ube2g2, Faf2, Syvn1, Sel1l, Aup1, and Derl2) [29] and exploiting ERAD to degrade PD-L1 expression on the cancer cell surface [30]. This evidence concerns the gene SEL1L and cancer.