A previous study showed that CD38 is highly expressed in HCC, and EVs/siCD38 inhibit CD38 enzyme activity, decrease adenosine production, and promote macrophage repolarization to the M1 type, thereby inhibiting HCC cell growth and metastasis in vitro and tumor growth in mice and overcoming PD-1/PD-L1 inhibitor resistance[223]. This evidence concerns the gene CD38 and neoplasm.