Targeted therapy, as the name implies, is like shooting a gun at a target in front of you, firing the bullet precisely to destroy the target and avoid injuring others. The “target” that targeted drugs attack is usually the abnormal gene that causes the disease to occur. Let’s talk about how the abnormal genes of slow-growing particles are created. The human body has 23 chromosomes, and if chromosome 9 and chromosome 22 are exchanged, a new chromosome 22 is created, which we call the Philadelphia chromosome. The Philadelphia chromosome is like a small boat that carries several genes, and because of the aforementioned “swap”, a new crew member appears on board – the bcr/abl fusion gene. The protein encoded by the bcr/abl fusion gene is a type of “tyrosine kinase”, which causes the hematopoietic stem cells to rapidly reproduce themselves and “immortalize” themselves, thus producing a large number of useless blood cells, and slow granulation occurs! Therefore, the “target” of slow granulation therapy is the bcr/abl fusion gene, and the “bullet” is our targeted drug, which can target the protein produced by the bcr/abl fusion gene to selectively kill leukemia cells. Normal cells are not affected by this targeted drug because the bcr/abl fusion gene is not present. In other words, the protein produced by the bcr/abl fusion gene sends a signal that causes cells with this protein to multiply faster than normal cells and not to die on their own, thus producing a large number of abnormal leukemic cells. If this signal is turned off, these leukocytes will die and the slow granules will be controlled. The targeted drug is the switch that turns off the protein signal. We know that slow granules can be divided into three phases: the chronic phase, the accelerated phase, and the acute phase. Patients in the chronic phase can survive for a long time, while those in the accelerated and acute phases may die quickly. Initial studies concluded that targeted therapy in patients with slow-growing granulocytes could keep the disease in the chronic phase for a long time, but could not cure the disease, a notion that has been challenged in recent years. The defects of hydroxyurea and interferon treatment for slow-onset granulocytes: Before the creation of targeted drugs, slow-onset granulocytes were commonly treated with hydroxyurea, which can only temporarily lower the indicators of white blood cells and platelets in the patient’s blood, creating the illusion that the disease is cured, but the leukemia cells continue to be produced, and eventually the patient will still enter the acute phase and die, so this approach only treats the symptoms but not the disease. Interferon treatment for slow-onset leukemia can reduce the number of white blood cells and the number of Philadelphia chromosomes, which can delay the onset of acute changes to a certain extent, but the leukemia cells will not disappear completely, and the patient will still die from acute changes. Neither hydroxyurea nor interferon therapy can prevent patients from entering the accelerated phase. Moreover, with the prolongation of hydroxyurea treatment, the remaining leukocytes in the patient’s body are not the same as they were at the beginning, and they will develop genetic mutations and become resistant to drugs, even to targeted drugs. Therefore, it is very dangerous to try to use traditional treatment first and then switch to targeted drugs when the treatment is ineffective, as patients may be resistant to targeted drugs at the same time, thus missing the best time for treatment. The long-term survival rate of patients is high with targeted drug therapy: The mortality rate of patients with lp treated with targeted drugs has been reduced to 10% or even lower, and 90% of patients can survive for a long time, avoiding patients to enter the acute stage to the maximum extent. Therefore, it is recommended that patients should apply targeted drug therapy directly after the diagnosis of slow granulation, and should not switch to targeted drugs after hydroxyurea or interferon therapy is ineffective, missing the best time for treatment.