In this sense, and although the inactivation of PFKFB3 is regarded as a promising therapeutic opportunity across several types of cancer (24, 40), we hypothesize that the balanced induction of this enzyme specifically in immune cells may instead represent a valuable strategy benefiting patients suffering from IPA, especially those harboring loss-of-function SNPs in PFKFB3. Accordingly, the activation of PFKFB3 has been shown to accelerate disease progression in models of sepsis (27). This evidence concerns the gene PFKFB3 and Ito hypomelanosis.