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AI is going full on dog-pile to the growing indications list…CCR5 made the very short AI generated list when looking for drugs that might impact aging:

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Three or four years ago I said that leronlimab may become a panacea for old age.

From the paper -

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According to the results, there were 9 genes common for all of 14 diseases and aging, specifically VHL, EGF, PTH, RET, BRCA1, SRC, CCR5, MIP, TNF

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Instead of targeting all of these factors with drugs individually one only needs to effectively block CCR5. The wonder that is leronlimab.

Already on the leronlimab regulator list are EGF, SRC, TNF and MIP-1a (CCL3) and MIP-1b (CCL4) which are downregulated. VHL activates overexpression of HIF-1a which is also on the list as being downregulated. PTH increases calcium levels in disease states, most likely leronlimab's downregulation of CA-2+ would mediate that. Leronlimab does not seem to downregulate RET but does downregulate what it increases - PI3K/AKT, RAS, RAF, MAPK, and PLC. BRAC1 repairs damaged DNA, CCR5 blockade stops the repairs from occurring.