The abnormal activation of RABs, including RAB5, RAB7, and RAB22, leads to abnormal endosomal trafficking [25], increased internalization and degradation of E-cadherin [29], increased epithelial-to-mesenchymal transition [29], uncontrolled cell growth [30], and subsequent gingival fibromatosis [19] (Figure 8). Here, RAB5A is linked to hereditary gingival fibromatosis.