KLB and metabolic dysfunction-associated steatohepatitis: Dissect the contribution of direct actions of FGF21 and FGF19 on the liver in NASH resolution and fibrosis:  In which cells are FGF receptor subtypes co-expressed with KLB in healthy and diseased livers?  What is the impact of FGFR4/KLB mediated effects on NASH resolution and fibrosis vs FGFR1c/KLB mediated effects (effect of FGFR4 vs FGFR1c specific FGF19 analogues in pre-clinical models)?  What is the contribution of FGFR2c/KLB and FGFR3c/KLB activation by FGF19/FGF21 in NASH?  Are the beta KLB CNS and adipose tissue specific ko models more prone to develop NASH?