chip were 2.3 times more likely to have a heart attack, or 4.4 times as likely if the variant allele frequency in their blood was greater than 0.10, than matched controls without chip. it has also been found that there is an increased risk of cardiovascular mortality in patients who exhibit chip and receive self-derived stem cell transplantation. the idea of chip having a causal role in human heart attacks/strokes has been given support by a 2017 study that showed impairment of the tet2 chip gene in mice causally led to accelerated atherosclerosis, and this finding in mice has been independently validated. the possibility of somatic mutations in the blood contributing not only to cancer risk but also to heart attack and stroke has generated much discussion in top-level scientific publications and a large multi-cohort study published in 2017 appears to confirm the causal link between chip and cardiovascular disease in humans. comorbidities in addition to its effects on those who would otherwise be considered healthy, chip may have implications in certain disease contexts. it has been shown that patients with chip who receive autologous stem cell transplantation (asct) as part of their treatment for lymphoma have worse outcomes than patients without chip. the poorer prognosis for these patients is due to both an increase in subsequent therapy-related myeloid neoplasms and increased risk for cardiovascular mortality. treatment there are currently no therapies for slowing or targeting chip mutations. together with the fact that progression from chip to outright hematologic malignancy remains infrequent, medical experts have argued against preemptive screening for chip but suggest routine follow-up for incidental chip findings. associated disorders clonal hematopoiesis is sometimes compared to the unrelated blood disorders of monoclonal gammopathy of undetermined significance (mgus) and monoclonal b-cell lymphocytosis (mbl) to which it bears similarities in its apparent priming for more advanced hematologic disease combined with a lack of symptoms and overall low risk of progression. the acquisition of additional mutations can cause chip to transform into the related blood disorders mds and aml.