One plausible explanation is the chronic inflammatory state associated with CML [25,26,27], characterized by elevated pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) that are known to suppress CYP3A expression and activity [28,29,30,31]. This evidence concerns the gene IL6 and chronic myelogenous leukemia, BCR-ABL1 positive.