# SensRORing cholesterol to drive protumoral myelopoiesis

## TL;DR

This paper shows how cholesterol activates RORγ to promote immune evasion in cancer, offering new strategies to enhance cancer immunotherapy.

## Contribution

The study identifies a cholesterol-driven RORγ pathway as a novel mechanism for protumoral myelopoiesis and immunosuppression.

## Key findings

- Cholesterol activates RORγ to drive expansion of MDSCs and TAMs.
- RORγ-dependent myelopoiesis leads to defective antitumor immune responses.
- Targeting RORγ and PCSK9 could improve cancer immunotherapy outcomes.

## Abstract

Protumoral myelopoiesis is a determinant of immunoevasion and tumor spread in many malignancies. In a recent issue of Cancer Discovery, Bleve and colleagues point to cholesterol‐driven RORγ activation as the molecular trigger of myeloid‐derived suppressor cells (MDSCs) and tumor‐associated macrophages (TAMs) expansion, resulting in defective antitumor response and disease progression.

Bleve et al. uncover a cholesterol‐driven immune evasion pathway, where RORγ‐dependent myelopoiesis shapes tumor immunosuppression. Targeting RORγ and PCSK9 emerges as a strategy to boost cancer immunotherapy.