The supporting evidence includes: (1) the association between increased macrophage infiltration and proliferation of GALNT14-expressing BCCs in vivo; (2) the requirement of GALNT14 in macrophage-induced growth of BCCs; (3) the ablation of this growth advantage upon the pharmacological inhibition or genetic knockdown of FGFR1 and 3; (4) the loss of macrophage-induced BCC growth upon the depletion of FGF2 in macrophages; and (5) the GALNT14-mediated glycosylation of FGFR1. Here, FGFR1 is linked to skin basal cell carcinoma.