However, our study generates two essential and provocative hypotheses that warrant further investigation: (a) ICB and inflammatory-CH (iCH; DNMT3A/TET2 related CH) share a bidirectional relationship where iCH may enhance the response to ICB and the response to ICB further drives iCH (as these mutant clones thrive under inflammation); (b) ICB-mediated iCH expansion may lead to a novel therapy-related myeloid neoplasm as patients on ICB therapies continue to live longer. This evidence concerns the gene TET2 and myeloid neoplasm.