Interestingly, Braig et al. (2014) reported that telomere shortening in the progression of CML is accompanied by a telomere-associated secretory phenotype (TASP), and the authors suggested that RAP1 might activate candidate NF-κB-dependent genes (e.g., CCL4, IL-6, IL-8) responsible for the inflammatory environment in cells with short, but not critically short telomeres [70]. Here, TERF2IP is linked to chronic myelogenous leukemia, BCR-ABL1 positive.