In retrospect, a majority of FDA-approved targeted cancer drugs exploit overactivated receptor tyrosine kinases triggering aberrant signaling cascades (aforementioned NTRK- and RET-involved fusions) or oversecreted growth factors stimulating environmental components (colony-stimulating factor 1, CSF1R, which will be discussed later in this review) generated by gene fusions as druggable vulnerabilities. The gene discussed is CSF1; the disease is cancer.