In poorly differentiated cSCC, VEGF is reportedly highly expressed and correlated with p16 expression, which suggests an interaction between VEGF and p16 in the dedifferentiation of cutaneous tumours.33 VEGF also has been implicated in tumour immune evasion by disabling myeloid dendritic cells.34 Blocking neuropilin‐1, which is a co‐receptor of VEGF in cutaneous cancer stem cells, impedes cancer stemness and renewal.35 Our study showed that C3a treatment increased cellular VEGF expression and secretion in the supernatants of A431 and SCC13 cells. This evidence concerns the gene VEGFA and cancer.