It has been proposed that LPA produced due to surgical wounds could contribute to the recurrence of gingival overgrowth by upregulating CCN2 expression in HGFs, an effect that is mediated by Smad3 and JNK activation and ALK5 transactivation [130], further highlighting the role of JNK in regulating cellular responses in gingival overgrowth. This evidence concerns the gene SMAD3 and gingival overgrowth.