Philippe Ravassard and colleagues have successfully derived functional human pancreatic beta cells. They used a sequential method involving transducing human fetal pancreases with an immortalizing factor to prevent senescence, followed by grafting into SCID mice for proliferation and differentiation into beta cells. The derived cells expressed characteristic beta cell markers, secreted insulin in response to glucose stimulation, and ameliorated chemically induced diabetes in a mouse model, demonstrating their functionality. The ΔF508 mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) is the most common cause of cystic fibrosis. A new study shows that this mutant CFTR can be transported to the plasma membrane via an unconventional secretion pathway mediated by Golgi reassembly stacking proteins (GRASPs). This pathway involves the activation of the unfolded protein response (UPR) by inositol-requiring protein 1 (IRE-1). GRASP upregulation rescued the mutant CFTR without inducing ER stress, and transgenic expression of GRASP in mice increased survival. This finding suggests a potential drug strategy for treating cystic fibrosis. Human cytomegalovirus (CMV) can incorporate the antibody MSL-192, which normally blocks CMV infection, and use it to infect new cells. This resistance is reversible and does not involve genetic changes. Instead, the antibody is taken up by CMV-infected cells and incorporated into assembling virions during maturation. The Fc domain of the incorporated MSL-192 is then used by CMV to infect nonimmune cells. This mechanism provides insight into a previously undescribed form of viral escape. - **Cell-to-cell spread of HIV**: Sigal et al. propose a model explaining how HIV can maintain a reservoir despite antiretroviral therapy through cell-to-cell spread. - **Schizophrenia**: A genome-wide association study identified five new loci associated with schizophrenia. - **Bipolar disorder**: A large-scale genome-wide association analysis identified a new susceptibility locus near the *ODZ4* gene. - **Proteomic comparison of human ES and iPS cells**: Phanstiel et al. used mass spectrometry to compare the proteomes of human embryonic stem cells and induced pluripotent stem cells, showing small differences in protein expression. - **APOBEC3G and NK cell recognition**: Norman et al. characterized an intrinsic antiviral mechanism where APOBEC3G enhances the recognition of HIV-infected primary T cells by natural killer cells.Philippe Ravassard and colleagues have successfully derived functional human pancreatic beta cells. They used a sequential method involving transducing human fetal pancreases with an immortalizing factor to prevent senescence, followed by grafting into SCID mice for proliferation and differentiation into beta cells. The derived cells expressed characteristic beta cell markers, secreted insulin in response to glucose stimulation, and ameliorated chemically induced diabetes in a mouse model, demonstrating their functionality. The ΔF508 mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) is the most common cause of cystic fibrosis. A new study shows that this mutant CFTR can be transported to the plasma membrane via an unconventional secretion pathway mediated by Golgi reassembly stacking proteins (GRASPs). This pathway involves the activation of the unfolded protein response (UPR) by inositol-requiring protein 1 (IRE-1). GRASP upregulation rescued the mutant CFTR without inducing ER stress, and transgenic expression of GRASP in mice increased survival. This finding suggests a potential drug strategy for treating cystic fibrosis. Human cytomegalovirus (CMV) can incorporate the antibody MSL-192, which normally blocks CMV infection, and use it to infect new cells. This resistance is reversible and does not involve genetic changes. Instead, the antibody is taken up by CMV-infected cells and incorporated into assembling virions during maturation. The Fc domain of the incorporated MSL-192 is then used by CMV to infect nonimmune cells. This mechanism provides insight into a previously undescribed form of viral escape. - **Cell-to-cell spread of HIV**: Sigal et al. propose a model explaining how HIV can maintain a reservoir despite antiretroviral therapy through cell-to-cell spread. - **Schizophrenia**: A genome-wide association study identified five new loci associated with schizophrenia. - **Bipolar disorder**: A large-scale genome-wide association analysis identified a new susceptibility locus near the *ODZ4* gene. - **Proteomic comparison of human ES and iPS cells**: Phanstiel et al. used mass spectrometry to compare the proteomes of human embryonic stem cells and induced pluripotent stem cells, showing small differences in protein expression. - **APOBEC3G and NK cell recognition**: Norman et al. characterized an intrinsic antiviral mechanism where APOBEC3G enhances the recognition of HIV-infected primary T cells by natural killer cells.