Considering that this role of Schwann cells in the modulation of cancer-associated pain has been correlated, at least in some circumstances, to the production of chemokines (M-CSF, TNF-α, and IL-6) which are abundant in the SASP of senescent cells, the discovery that Schwann cells can undergo senescence discloses further conceivable mechanisms of pain generation and, at the same time, new possible opportunities for the management of cancer-evoked pain (146–148). The gene discussed is CSF1; the disease is cancer.