I'll let ohm chime in as he knows the pathways incredibly well but just to point out that Polycythemia Vera Leukemia is a type of myeloproliferative neoplasms (MPN). This article seems to go into depth with regards to this type of blood cancer and cytokines

https://www.sciencedirect.com/science/article...3219300047

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The data summarized above clearly demonstrate that MPN-associated oncogenes can trigger inflammatory responses of both the malignant and nonmalignant cells. However, it is conceivable that chronic inflammation itself may lead to an MPN.

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Furthermore, a quick scan of the literature and it looks like inhibiting JAK1 and JAK2 has been studied

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These data suggest that inhibition of JAK1 and JAK2 by ruxolitinib can efficiently reduce the malignant clone in some MF patients, potentially by removing some of the MPN-promoting cytokines such as TNF-α, but that it additionally antagonizes inflammatory processes in nonmalignant cells

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Further data from mouse models suggest that a stronger inhibition of the mutant JAK2 protein or its signal transduction pathways, either by genetic ablation of JAK2 or by combination of ruxolitinib with other drugs, may improve the treatment of MPNs

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Based on ohm's oft quoted list

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leronlimab regulates -

MapK, Erk 1 and 2, Jak 1, 2 and 3, ATP, mTORc1, TNF-a, TNFSF14, IFNy, NF-kb, bradykinin, NETosis, neuropin-1, PI3k, GM-CSF, IL1b, IL-2, IL-4, IL-6, IL-8, IL-10, IL-13, IL-17, CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL11, CCL13, CCL14, CCL16, VEGF, SYK, SHP1, SHP2, PD-1, C5a, CA-2+,CD38, collagen, macrophage differentiation, TGF-b

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We know that leronlimab does target JAK1/2. Curious to hear what ohm has to add, but I had looked at blood cancers before so wanted to share what I had found.

Sorry to hear that your friend is going through this. Wishing him/her healing thoughts!!!