SOAT1 and Epstein-Barr virus infection: In summary, frequent genetic alterations of the chromosome 9p24.1 locus (amplification, copy gain, polysomy, rearrangement), constitutive activation of the JAK/STAT pathway, and EBV infection lead to PD-L1/L2 overexpression in CHL and resultant tumor evasion from immune surveillance (Table 1).