NFKB1 and lung disorder: We previously reported the generation of iPSCs from patients with SFTPCI73T variants and lung disease (27) and identified that expression of mutant SP-CI73T in iAT2s results in diminished AT2 cell progenitor function, autophagy perturbations, altered bioenergetic programs, time-dependent increased glycolysis, and activated canonical NF-κB signaling (27).