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Purpose This paper aims to apply the ACRL Framework for Information Literacy for Higher Education frame Information Creation as a Process to encourage student confidence in government information. This approach will also help librarians address the continued erosion of trust in government exacerbated by campaigns of mis- and disinformation waged by the 45th President. Design/methodology/approach The authors examined recent literature on the public’s increased distrust of government under the 45th President, the impact of extreme skepticism on students, and the role instruction and government information librarians can play in addressing these issues. The authors used the ACRL Framework for Information Literacy for Higher Education frame Information Creation as a Process as a guide for teaching students about the complexities of government information creation processes and addressing student apprehension about utilizing government information in their academic research. Findings Research indicates that in the midst of a decline in public trust in government, librarians are fighting an uphill battle to encourage wary students to use government information for academic research. Librarians can combat this via targeted Framework-aligned instruction. An example of how the frame Information Creation as a Process can be applied to government information is presented. Practical implications For easy implementation of the ideas presented in this paper, learning outcomes and a sample lesson plan are provided. Originality/value This paper contributes to the library literature on government information literacy and instruction as well as the Framework. It is the only paper that addresses the application of the frame Information Creation as a Process to government information.

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<div>Abstract<p>Expression of the TAM (TYRO3, AXL, MER) family of receptor tyrosine kinases (RTK) has been associated with cancer progression, metastasis, and drug resistance. In immune cells, TAM RTKs can dampen inflammation in favor of homeostatic wound-healing responses, thus potentially contributing to the evasion of cancer cells from immune surveillance. Here we characterize the small-molecule RXDX-106 as a selective and potent pan-TAM RTK inhibitor with slow dissociation kinetics and significant antitumor activity in multiple syngeneic tumor models. Expression of AXL and MER on both immune and tumor cells increased during tumor progression. Tumor growth inhibition (TGI) following treatment with RXDX-106 was observed in wild-type mice and was abrogated in immunodeficient mice, suggesting that the antitumor activity of RXDX-106 is, in part, due to the presence of immune cells. RXDX-106–mediated TGI was associated with increased tumor-infiltrating leukocytes, M1-polarized intratumoral macrophages, and activation of natural killer cells. RXDX-106 proportionally increased intratumoral CD8⁺ T cells and T-cell function as indicated by both IFNγ production and LCK phosphorylation (pY393). RXDX-106 exhibited its effects via direct actions on TAM RTKs expressed on intratumoral macrophages and dendritic cells, leading to indirect activation of other immune cells in the tumor. RXDX-106 also potentiated the effects of an immune checkpoint inhibitor, α-PD-1 Ab, resulting in enhanced antitumor efficacy and survival. Collectively, these results demonstrate the capacity of RXDX-106 to inhibit tumor growth and progression and suggest it may serve as an effective therapy against multiple tumor types.</p>Significance:<p>The pan-TAM small-molecule kinase inhibitor RXDX-106 activates both innate and adaptive immunity to inhibit tumor growth and progression, indicating its clinical potential to treat a wide variety of cancers.</p></div>

<p>GO analysis of RNA-Seq data from the MC38 combination study</p>