In recent decades, the dermatoscope has been thought to be an essential tool for skin cancer diagnosis, and it is currently referred as the “dermatologist’s stethoscope.”^1-3 However, in some cases the diagnosis of malignant abnormalities is still challenging in a subset of difficult-to-diagnose melanomas (MMs) and nonmelanoma skin cancers. To narrow this gray zone, reflectance confocal microscopy (RCM), a second-level in vivo imaging technique, has proven to be a useful tool in saving unnecessary excisions of benign lesions that can look dermoscopically suspicious for skin cancer while catching MMs that are dermoscopically inconspicious.^4-8 Reflectance confocal microscopy provides a horizontal visualization of the skin at a nearly histological resolution and is currently a validated instrument for noninvasive diagnosis of skin tumors, already counting over 600 indexed articles.^4-15

For a long time the relationship between inflammatory bowel diseases (IBDs) and psoriasis has been investigated by epidemiological studies. It is only starting from the 1990s that genetic and immunological aspects have been focused on. Psoriasis and IBD are strictly related inflammatory diseases. Skin and bowel represent, at the same time, barrier and connection between the inner and the outer sides of the body. The most important genetic correlations involve the chromosomal loci 6p22, 16q, 1p31, and 5q33 which map several genes involved in innate and adaptive immunity. The genetic background represents the substrate to the common immune processes involved in psoriasis and IBD. In the past, psoriasis and IBD were considered Th1-related disorders. Nowadays the role of new T cells populations has been highlighted. A key role is played by Th17 and T-regs cells as by the balance between these two cells types. New cytokines and T cells populations, as IL-17A, IL-22, and Th22 cells, could play an important pathogenetic role in psoriasis and IBD. The therapeutic overlaps further support the hypothesis of a common pathogenesis.