To understand the immune mechanisms activated by mIL12 mRNA that underpin the strong tumor inhibition despite deficient antigen presentation in both Yummer1.7 and MC38 B2M KO tumors, we performed pharmacodynamic studies by replicating the study design and treatment regime as for efficacy experiments above, but the studies were terminated early when the tumors were in an active response state. This evidence concerns the gene B2M and neoplasm.