Among these, a connection of both TNFRSF12A and CD38 proteins to AKT1 is remarkable, as the stimulation of IGF1/AKT1 axis via the targeting of p16-induced senescence was recently shown to alleviate at least some phenotypic features of COPD (Cottage et al., 2019). The gene discussed is TNFRSF12A; the disease is chronic obstructive pulmonary disease.