Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

[Q]: Although peak finding in next-generation sequencing (NGS) datasets has been addressed extensively, there is no consensus on how to analyze and process biological replicates. Furthermore, most peak finders do not focus on accurate determination of enrichment site widths and are not widely applicable to different types of datasets. We developed JAMM (Joint Analysis of NGS replicates via Mixture Model clustering): a peak finder that can integrate information from biological replicates, determine enrichment site widths accurately and resolve neighboring narrow peaks. JAMM is a universal peak finder that is applicable to different types of datasets. We show that JAMM is among the best performing peak finders in terms of site detection accuracy and in terms of accurate determination of enrichment sites widths. In addition, JAMM's replicate integration improves peak spatial resolution, sorting and peak finding accuracy. JAMM is available for free and can run on Linux machines through the command line: [Link]
[A]: Which peak calling algorithm employs mixture model clustering under the hood?


[Q]: NeXTSTEP (also stylized as NeXTstep, NeXTStep, and NEXTSTEP) is a combination of several parts: a Unix operating system based on the Mach kernel, plus source code from BSD Display PostScript and a proprietary windowing engine the Objective-C language and runtime an object-oriented (OO) application layer, including several ''kits'' development tools for the OO layers NeXTSTEP is notable for having been a preeminent implementation of the latter three items.
[A]: What is the programming language for NeXTSTEP?


[Q]: The TNF family member receptor activator for NF-B ligand (RANKL) and its receptors RANK and osteoprotegerin are key regulators of bone remodeling but also influence cellular functions of tumor and immune effector cells. In this work, we studied the involvement of RANK-RANKL interaction in NK cell-mediated immunosurveillance of acute myeloid leukemia (AML). Substantial levels of RANKL were found to be expressed on leukemia cells in 53 of 78 (68%) investigated patients. Signaling via RANKL into the leukemia cells stimulated their metabolic activity and induced the release of cytokines involved in AML pathophysiology. In addition, the immunomodulatory factors released by AML cells upon RANKL signaling impaired the anti-leukemia reactivity of NK cells and induced RANK expression, and NK cells of AML patients displayed significantly upregulated RANK expression compared with healthy controls. Treatment of AML cells with the clinically available RANKL Ab Denosumab resulted in enhanced NK cell anti-leukemia reactivity. This was due to both blockade of the release of NK-inhibitory factors by AML cells and prevention of RANK signaling into NK cells. The latter was found to directly impair NK anti-leukemia reactivity with a more pronounced effect on IFN- production compared with cytotoxicity. Together, our data unravel a previously unknown function of the RANK-RANKL molecule system in AML pathophysiology as well as NK cell function and suggest that neutralization of RANKL with therapeutic Abs may serve to reinforce NK cell reactivity in leukemia patients.
[A]:
To the ligand of which receptors does Denosumab (Prolia) bind?