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ABSTRACTThis article attempts to decode the ways in which social policy that has essentially developmental and welfare imperatives is being used to pursue an exclusivist‐authoritarian right‐wing agenda in India under Narendra Modi. The authors highlight a contradistinction between the previous United Progressive Alliance regime led by the Congress Party and the current National Democratic Alliance regime led by the BJP to show the shift in the understanding and the role of social policy. In essence, social programmes have been combined with market‐oriented reforms, undoing the entitlements‐based approach to social policies of the previous regime. The authors then go on to discuss a variety of social policy programmes introduced by the Modi government with a focus on public health and sanitation objectives, but also including gender empowerment imperatives, education, training and employment programmes for socially marginalized groups.

© 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works Diamond-Blackfan anemia (DBA) is a rare hematopoietic disease characterized by a block in red cell differentiation. Most DBA cases are caused by mutations in ribosomal proteins and characterized by higher than normal activity of the tumor suppressor p53. Higher p53 activity is thought to contribute to DBA phenotypes by inducing apoptosis during red blood cell differentiation. Currently, there are few therapies available for patients with DBA. We performed a chemical screen using zebrafish ribosomal small subunit protein 29 (rps29) mutant embryos that have a p53-dependent anemia and identified calmodulin inhibitors that rescued the phenotype. Our studies demonstrated that calmodulin inhibitors attenuated p53 protein amount and activity. Treatment with calmodulin inhibitors led to decreased p53 translation and accumulation but does not affect p53 stability. A U.S. Food and Drug Administration-approved calmodulin inhibitor, trifluoperazine, rescued hematopoietic phenotypes of DBA models in vivo in zebrafish and mouse models. In addition, trifluoperazine rescued these phenotypes in human CD34+ hematopoietic stem and progenitor cells. Erythroid differentiation was also improved in CD34+ cells isolated from a patient with DBA. This work uncovers a potential avenue of therapeutic development for patients with DBA.