My PhD was conducted under the supervision of Pr. Jean-Luc Taupin in Bordeaux (France), where I studied the role of CD95/CD95L pair in immune homeostasis. CD95, also known as Fas is a death receptor that belongs to the Tumor Necrosis family (TNF) receptor family. In the presence of its ligand designated CD95L or FasL, CD95 implements an apoptotic signalling pathway contributing to the immune surveillance and immune tolerance 1-4. Then, I joined Pr. Marcus Peter’s laboratory at University of Chicago (2002-2005, Chicago, USA) where we established that the stimulation of CD95 in cancer cells resistant to the CD95-mediated apoptotic signalling pathway, promoted carcinogenesis through the induction of non-apoptotic signals 5-7. In 2005, I have been hired as an Assistant professor by INSERM (“chargé de recherche” Inserm from 2005 to 2012, France). INSERM is a National health research institute operating under the French Ministries of Health and Research. In Bordeaux, I created my research group and established that anti-tumour agents induced rapid redistribution of CD95 into lipid rafts to facilitate the implementation of the apoptotic signalling pathway and the elimination of malignant cells 8,9. In 2010, I moved to University of Rennes (Rennes, France) and as a “director of research” Inserm (Full Professor) joined the Comprehensive Cancer Center Eugène Marquis in Rennes (France) to create an INSERM Unit working on death receptors, inflammation and tumor adaptation. CD95L belongs to the TNF superfamily and this transmembrane cytokine can be shed by metalloproteases to release in bloodstream a soluble ligand (s-CD95L). Our work highlighted that s-CD95L i) is increased in systemic lupus erythematosus (SLE) and triple negative breast cancer (TNBC) patients and ii) participates in the severity of these pathologies by promoting the Th17 trafficking in the inflamed organs 10,11 or the metastatic dissemination of TNBC cells, respectively 12. In addition, my Team demonstrated that in the presence of s-CD95L, CD95 elicits the formation of a molecular complex that we termed MISC, for Motility-Inducing Signalling Complex, thereby inducing a non-orthodox c-yes/Orai1/Ca2+/PI3K signalling pathway 10,12,13. Currently, my group including surgeons, clinicians, biologists, chemists and scientists is interested to understand how the “apoptotic receptor” CD95 participates in the aggravation of the clinical outcomes in chronic inflammatory disorders 10,11,13 and breast cancers 12,14. In collaboration with chemists and modelers, we recently synthesized original peptidomimetics selectively inhibiting the CD95-mediated pro-inflammatory response without affecting its apoptotic signal, which is instrumental in controlling the immune response 15. In parallel, I founded a company called APOFASBiotech (2017), which aims at accompanying the original CD95 inhibitors whose therapeutic activity has been validated in different lupus-prone animal models to clinical trials.