found that the homologous to the E6-AP carboxy terminus domain and RCC1-like domain 2 (HERC2) promote inflammation-induced stemness and immune evasion in HCC cells through JAK2/STAT3 signaling, the underlying mechanism of which is related to the regulatory effect of HERC2 on JAK2/STAT3 signaling participating in the crosstalk between cancer stemness and immune evasion (150). The gene discussed is HERC2; the disease is cancer.