CSF1R, paradoxically associated with favorable prognosis in DLBCL, remains a therapeutic target for reprogramming M2-tumor-associated macrophages (TAMs), as shown by SYHA1813’s (a VEGFR and CSF1R inhibitor) efficacy against Bruton’s tyrosine kinase inhibitor (BTKi) resistance [30]. The gene discussed is CSF1R; the disease is diffuse large B-cell lymphoma.