Such a phenotypic switch driven by lactic acidosis was accompanied by a modest but significant increase in the mRNA expression of the pro-inflammatory cytokines IL-6, IL-1β, and TGFβ1, which in turn could account at least in part for the ability of acid-adapted acADSCs to induce the activation of normal fibroblasts. The gene discussed is IL1B; the disease is lactic acidosis.