The acceptable CRS and ICANS rates may be attributed to the use of an enhanced conditioning regimen and ASCT before CAR T-cell infusion to minimize the tumor burden and myeloid cells, which have been confirmed to be related to the occurrence and severity of CRS and ICANS [39–41]; moreover, myeloid cell-derived cytokines (IL-1, IL-6, GM-CSF, etc.)were the major sources of CRS after CAR T-cell immunotherapy [42–44]. This evidence concerns the gene IL6 and congenital rubella syndrome.