In conclusion, the experimental studies reported to date have found that both JAK2V617F mutant cells and different CALR-mutated clones (bearing either type 1 or type 2 frameshift mutations, resulting in “non-self” C-terminal sequences of calreticulin protein) ultimately generate a few distinct highly immunogenic peptides, broadly shared by the majority of MPN patients, thus representing optimal neoantigens which directly provide the opportunity to develop mutant-specific adoptive CTL therapies and vaccination strategies [128,129,130]. Here, CALR is linked to myeloproliferative disorder.