There are three overarching phases and implications of these findings as follows: an intrinsic resistance response to T-cell related heterozygous germline alterations (e.g., UNC13D, CX3CR1 mutations), followed by an extrinsic high antigen-driven T cell dysfunction measured by higher LDH level before leukapheresis, finally with the manifestation of low CRS severity (Figure 5). This evidence concerns the gene CX3CR1 and congenital rubella syndrome.