More recently, Li et al. described a homozygous splice site mutation in LCK (c.188-2A>G), predicted to affect the 3’ splice acceptor site of LCK exon 4, in a consanguineous family presenting with a partial CD4+ T-cell defect, and susceptibility to human papillomavirus (HPV) infections with atypical epidermodysplasia verruciformis (EV), as well as recurrent pneumonia [2]. This evidence concerns the gene LCK and pneumonia.