Given that both common acne vulgaris and EGFRi-induced eruptions occur in sebum-rich regions of the body that are colonized with C. acnes, and that C. acnes is known to be involved in the pathogenesis of acne (19–22), we exposed PHKs to both erlotinib and C. acnes. Interestingly, IL-36γ production at the mRNA and protein level was further enhanced (8.4-fold in mRNA, P = 0.001) when PHKs were simultaneously exposed to erlotinib and C. acnes (Figure 1, D and E). This evidence concerns the gene IL36G and acne.