Specifically, Chen et al. demonstrated that EPHB1 was post-translationally modified by the small ubiquitin-like modifier (SUMO) protein at lysine residue 785, with the SUMOylation resulting in the inhibition of EPHB1 downstream signaling via protein kinase C gamma (PKCγ), and subsequently in the repression of tumor growth [105]. This evidence concerns the gene PRKCG and neoplasm.