More importantly, in pulmonary fibrosis models, simultaneous inhibition of both PI3K/AKT and CaMKII produces a stronger pro-apoptotic effect, significantly enhancing apoptosis in human lung fibroblasts (HLFs) and suppressing collagen expression—an effect superior to inhibiting either pathway alone (Zhao et al., 2020a). This evidence concerns the gene AKT1 and pulmonary fibrosis.