Gall induction requires the contact of the female ovipositor or mouthparts of gall-inducing herbivores with plant epidermal cells, the first line of contact between the two interactive organisms. Plant epidermal cells may react, emitting chemical defenses or isolating a small group of cells to eliminate invaders. Evidences indicate that tentative cell responses toward impairing the establishment of the inducer may be successful or not. If the reaction is toward defensive traits, plant cells will try to kill the egg or the larva via local secretion or trafficking of unpalatable or destructive metabolites from other plant parts to the site of contact with the plant-galling herbivore interaction. These metabolites prevent egg implantation or larval feeding, and epidermal cells exhibit local reactions. These reactions are true counterattacks, as they deter the success of the gall inducer offspring. Eliminating a group of cells by cell death processes is a common phenomenon that may be visualized as brownish spots, indicating the accumulation of phenolics, secondary metabolites whose presence is a local attempt to impair gall induction. If the egg or larvae can surpass these first reactions, epidermal cells divide and expand, new elongation axes may be assumed, and the signaling with the other cell types will differ from the ordinary pattern. The epidermal cells of the inner gall surface lining the gall chamber are under stronger cecidogenic stimuli and constitute the nutritive cells of most galls. In contrast, outer epidermal cells are usually hypertrophied and have modified or neoformed appendices. The new cell organization in the gall outer epidermis involves the inhibition or overexpression of trichoblasts, malformed stomata, a multilayered epidermis, the differentiation of lenticels, and the substitution of the epidermis by the periderm. Such anatomical diagnostic features imply new functional traits for the dermal system.