Eosinophilic airway inflammation is the most frequent pathophysiologic subtype of asthma, underpinned by type 2 (T2-high) allergic or non-allergic mechanisms and consisting of synergistic communications between innate and adaptive immune responses coordinated by both T helper 2 (Th2) lymphocytes and group 2 innate lymphoid cells (ILC2), which release interleukins 4 (IL-4), 13 (IL-13) and 5 (IL-5) [12,13,14]. This evidence concerns the gene IL13 and asthma.