In particular, an E3 ubiquitin ligase, Fbxo38, has been reported to interact with PD1 and mediate its K48 polyubiquitination and subsequent proteasomal degradation.98 T cell-conditional knockout of Fbxo38 results in increased surface expression of PD1 in T cells and impairs antitumor immunity, leading to more rapid tumor growth98 (Fig. 2). The gene discussed is FBXO38; the disease is neoplasm.