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Both K‐12 schools and STEM disciplines are embedded in White supremacy and exclusion, making it that much harder for Black women to maintain an interest and sense of belonging in STEM. Through a Critical Race Feminism methodology, we tell the counterstories of our two co‐authors, two Black women, over the course of their lives. Through these counterstories (stories that run counter to normative stories of STEM as male and White), Kelli and Samantha show us how they negotiated and maintained a sense of belonging in STEM even through moments of self‐doubt in their STEM trajectory. These negotiations allowed them to carve a space for themselves within STEM. A key finding from these counterstories was the resilience both women developed through their participation in counterspaces and support from family and teachers that helped them develop pride in their STEM identity trajectories. Our study adds to the research on Black women's journeys in STEM by describing resilience strategies that our authors were forced to develop in response to White supremacy and how they were able to maintain their STEM identity by creating a counterstory that allowed them to maintain their sense of belonging within STEM. And yet, we conclude by asking if resilience is enough since both women questioned their authentic and valued place in their respective STEM disciplines because of the dominant storyline of STEM as White and male. Their stories reveal the deeper truth that change is needed in STEM to empower students of color to see themselves as not just tolerated but valued members of the discipline. [ABSTRACT FROM AUTHOR]

Hybrid insulin peptides (HIPs) form in pancreatic β-cells through the formation of peptide bonds between proinsulin fragments and other peptides. HIPs have been identified in pancreatic islets by mass spectrometry and are targeted by CD4 T cells in patients with type 1 diabetes (T1D) as well as by pathogenic CD4 T-cell clones in nonobese diabetic (NOD) mice. The mechanism of HIP formation is currently poorly understood; however, it is well established that proteases can drive the formation of new peptide bonds in a side reaction during peptide bond hydrolysis. Here, we used a proteomic strategy on enriched insulin granules and identified cathepsin D (CatD) as the primary protease driving the specific formation of HIPs targeted by disease-relevant CD4 T cells in T1D. We also established that NOD islets deficient in cathepsin L (CatL), another protease implicated in the formation of disease-relevant HIPs, contain elevated levels of HIPs, indicating a role for CatL in the proteolytic degradation of HIPs. In summary, our data suggest that CatD may be a therapeutic target in efforts to prevent or slow the autoimmune destruction of β-cells mediated by HIP-reactive CD4 T cells in T1D. [ABSTRACT FROM AUTHOR]