Combining these two observations would suggest that in human IPF, there is endogenous inhibition of autophagy through mechanisms that may be reliant on changes in cellular ADP/ATP ratios or a potential cross-talk between apoptosis and autophagy (Bcl2-Beclin-1) [38,39,40,41] that, in turn, leads to reduced fibrosis and thus, improved (or better preserved) lung function (Figure 4C). The gene discussed is BCL2; the disease is idiopathic pulmonary fibrosis.