*2.1.2.1 Combined therapy*

Like other checkpoint inhibitors, although camrelizumab exhibits a high objective response rate in patients with r/r cHL, the CR rate remains low (as shown above). It has been proven that inhibition of *de novo* DNA methylation can boost T-cell function upon PD-1 blockade [83, 84]. Decitabine is a DNA demethylating agent [85]; therefore, clinical trial combining a low dose of decitabine with camrelizumab against r/r cHL was conducted (NCT02961101, NCT03250962). Indeed, when compared with camrelizumab monotherapy, r/r cHL patients receiving decitabine plus camrelizumab exhibited a higher CR rate (79% vs. 32%) and longer median PFS (35.0 vs. 15.5 months) [86, 87]. In addition, the administration of decitabine plus camrelizumab showed promising efficacy against HL with resistance to anti-PD-1 [86, 87]. Similarly, combination treatment of anti-angiogenic agent apatinib and camrelizumab might be a salvage option for r/r cHL patients who failed PD-1/PD-L1 inhibitor therapy, as demonstrated in the case reports presented by Yan et al. [88]*.* Out of seven enrolled patients, two achieved CR, and four achieved PR. The median PFS was 10 months, and no unexpected side effects were observed.
