一名46岁男性被诊断患有慢性粒细胞白血病（CML）慢性期。他接受了伊马替尼、尼罗替尼和达沙替尼治疗，但未能达到完全细胞遗传学缓解 (CCyR)。酪氨酸激酶抑制剂治疗后，检测到F317L BCR-ABL1激酶结构域突变。 66 岁时，患者开始服用 45 毫克/天的 ponatinib (PON)，并在三个月内达到了 CCyR。随后，由于动脉闭塞事件，PON 剂量逐渐减少至 15 mg，每周一次。 3 年深度分子反应（≥ MR4.5）后停止 PON。然而，患者在两个月内失去了 MR4.0，并重新开始 PON（15 mg 每周一次）。他在一个月内再次达到 MR4.0，然后在以相同的 PON 剂量开始透析治疗后达到更深的分子反应 (MR5.0)。 PON（15mg每周一次）的谷值为5.8ng/ml，抑制了CML克隆中的F317L突变。目前，患者77岁，维持MR5.0。慢性肾功能衰竭可能会导致接受 PON 的患者吸收过度和代谢迟缓。开始血液透析可以改善体内平衡，从而增强针对 CML 的抗肿瘤免疫力。

A 46-year-old man was diagnosed with chronic myeloid leukemia (CML) in chronic phase. He was treated with imatinib, nilotinib, and dasatinib, but failed to achieve a complete cytogenetic response (CCyR). After tyrosine kinase inhibitor therapy, F317L BCR-ABL1 kinase domain mutation was detected. At age 66, the patient started ponatinib (PON) at 45 mg/day, and achieved CCyR within three months. Subsequently, PON was tapered to 15 mg once weekly due to arterial-occlusive events. PON was discontinued after a 3-year deep molecular response (≥ MR4.5). However, the patient lost MR4.0 within two months, and PON (15 mg once weekly) was restarted. He achieved MR4.0 again within one month, and then a deeper molecular response (MR5.0) after starting dialysis therapy at the same PON dose. The trough value of PON (15 mg once weekly) was 5.8 ng/ml, which suppressed F317L mutation in the CML clone. Currently, the patient is 77 years old and is sustaining MR5.0. Chronic renal failure may cause hyperabsorption and metabolic retardation in patients receiving PON. Initiation of hemodialysis may improve homeostasis resulting in enhanced anti-tumor immunity against CML.