Percutaneous aortic balloon counterpulsation (IABP) was first used in 1968 after cardiac surgical bridgework to increase cardiac output by inflating the heart in diastole and reducing cardiac afterload by exhausting the heart in systole, which has been shown to increase diastolic coronary perfusion. Compared with other high profile left ventricular assist devices, IABP is more approachable, simple to operate and relatively inexpensive, especially for China, and is a must-have equipment for catheterization laboratories, and is also recommended as Class I for cardiogenic shock after acute myocardial infarction in developed countries such as the United States and Europe. However, a study published in the New Eng Journal in October 2012 has surprising results and has the potential to put IABP in the cold. This study was the well-known IABP-SHOCK2 study, the first multicenter, randomized, controlled study of the effect of an IABP ventricular assist device on early post-reconstruction hemodynamics after acute myocardial infarction complicated by cardiogenic shock. The primary endpoint of the study was 30-day mortality, and secondary endpoints were time to hemodynamic recovery, time and dose of vasoactive drug application, and complications, among others. A total of 600 patients from 37 hospitals in Germany were enrolled in the study, with 301 randomized to the IABP group compared to 299 in the control group. The results of the study showed no significant differences in the primary and secondary endpoints between the two groups. This result was a big surprise and confused people, with different interpretations by interventionalists and controversial clinical applications of IABP, and some may even say that IABP, which we have been chasing for years, is retiring from the history stage. However, it seems to be too much to kill IABP because of this one study. When we look back at several small, retrospective and registry studies, it is easy to find that most of these studies found IABP to be effective for non-reperfusion therapy or thrombolysis, while there is some disagreement about the adjuvant effect after early PCI. The question arises, since these studies concluded that IABP is beneficial in acute myocardial infarction without reperfusion therapy or with thrombolysis only, this suggests a mechanistic cardioprotective effect of IABP, but why is this effect not evident when combined with better PCI therapy? If you give a poor man a $100 bill, he will find it useful, but if you give the same amount of money to a millionaire, he will not think so, because early PCI effectively improves myocardial perfusion and significantly improves the mortality of patients, which to some extent dilutes the prognostic effect of IABP. But we should not think that IABP is useless, just as a hundred dollar bill is still positive for a millionaire, I think the cardioprotective effect of IABP is still unquestionable, perhaps we need a better evaluation criteria to judge the role of IABP, rather than just a simple and brutal means to give the death sentence to IABP by 30-day mortality.