叉头盒O (FOXO)转录因子是细胞存活和生长的关键调控因子。FOXO的转录活性和亚细胞定位受到翻译后修饰的严格调控。
2013年5月14日，H. Lee Moffitt癌症中心程金（音译，Jin Q Cheng）及北京大学肿瘤医院寿成超共同通讯在PLOS ONE 在线发表题为“IKBKE phosphorylation and inhibition of FOXO3a: a mechanism of IKBKE oncogenic function”的研究论文，该研究表明IKBKE主要通过SerS644的磷酸化调控FOXO3a，并且IKBKE至少在一定程度上通过调控FOXO3a发挥其细胞功能。
但是，在2023年7月25日，该文章被撤回，主要原因是文章存在伪造和/或捏造的数据的行为。
另外，2010年3月9日，H. Lee Moffitt癌症中心程金（音译，Jin Q Cheng）团队在PLOS ONE 在线发表题为“Regulation of proapoptotic mammalian ste20-like kinase MST2 by the IGF1-Akt pathway”的研究论文，该研究首次证明细胞外细胞生存信号IGF1调节MST2, Akt是MST2的关键上游调节因子。但是，在2023年7月25日，该文章被撤回，主要原因是文章存在伪造和/或捏造的数据的行为。
最后，诚信科研编辑部发现，在2016年Journal of Biological Chemistry 撤回了程金的19篇文章。
莫菲特癌症中心(Moffitt Cancer Center)对这篇文章进行了调查，并确定以下数据存在伪造和/或捏造的证据:图3E, pfoxo3a - s644面板，第1列；在它们被发现不当行为后，莫菲特癌症中心建议撤回[1]。PLOS编辑还注意到下面列出的附加面板中的图像不规范：图2A, HA-FOXO3a面板和Myr-IKBKE面板；图2B，左侧HA-FOXO3a面板和右侧Myr-IKBKE面板；作者没有回应关于上述担忧的编辑沟通，也没有提供任何基础数据。鉴于机构调查的结果，以及对这些数据的完整性提出质疑的多个图片小组的担忧，PLOS ONE 编辑撤回这篇文章。WT对此作出了回应，但对编辑的决定既不同意也不反对。JPG, SS, YX, CS和JQC要么没有直接回应，要么无法联系到。另外，由程金署名（通讯作者）的19篇Journal of Biological Chemistry 被撤回文章列表：[1]MicroRNA-221/222 negatively regulates estrogen receptor α and is associated with tamoxifen resistance in breast cancer.[2]Phosphoinositide 3-kinase/Akt inhibits MST1-mediated pro-apoptotic signaling through phosphorylation of threonine 120.[3]IKKϵ phosphorylation of estrogen receptor α Ser-167 and contribution to tamoxifen resistance in breast cancer.[4]A small molecule inhibits Akt through direct binding to Akt and preventing Akt membrane translocation.[5]MicroRNA-155 regulates cell survival, growth, and chemosensitivity by targeting FOXO3a in breast cancer.[6]Phosphorylation and activation of androgen receptor by Aurora-A.[7]IKBKE protein activates Akt independent of phosphatidylinositol 3-kinase/PDK1/mTORC2 and the pleckstrin homology domain to sustain malignant transformation.[8]Identification of Akt interaction protein PHF20/TZP that transcriptionally regulates p53.[9]MicroRNA MiR-214 regulates ovarian cancer cell stemness by targeting p53/Nanog.[10]Positive feedback regulation between Akt2 and MyoD during muscle differentiation. CLONING OF Akt2 PROMOTER.[11] Inhibition of JNK by cellular stress- and tumor necrosis factor α-induced AKT2 through activation of the NFκB pathway in human epithelial cells.[12]Phosphatidylinositol 3-kinase/Akt pathway regulates tuberous sclerosis tumor suppressor complex by phosphorylation of tuberin.[13]AKT2 inhibition of cisplatin-induced JNK/p38 and Bax activation by phosphorylation of ASK1. IMPLICATION OF AKT2 IN CHEMORESISTANCE.[14]Akt phosphorylation and stabilization of X-linked inhibitor of apoptosis protein (XIAP).[15]ArgBP2γ interacts with Akt and p21-activated kinase-1 and promotes cell survival.[16]Molecular cloning and characterization of the human AKT1 promoter uncovers its up-regulation by the Src/Stat3 pathway.[17]Akt attenuation of the serine protease activity of HtrA2/Omi through phosphorylation of serine 212.[18]Identification of Aurora-A as a direct target of E2F3 during G2/M cell cycle progression.[19]Activation of phosphatidylinositol 3-kinase/Akt pathway by androgen through interaction of p85α, androgen receptor, and Src.https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0289330
