Consistently, Cortes et al. [85] have shown that RHOA-G17V mutation drives proliferation and polarization of human follicular helper T lymphocytes (Tfh), which eventually culminate in AITL development with the upregulation of ICOS (inducible co-stimulator) and activation of PI3K/mitogen-activated protein kinase (MAPK) signaling pathways. Here, RHOA is linked to angioimmunoblastic T-cell lymphoma.