PNPLA2 and steatosis: These results indicate that the Ser33 residue is a crucial phosphorylation site of 17β-HSD13 for ATGL-mediated lipolysis in LDs and suggest that loss of PKA-mediated Ser33 phosphorylation of 17β-HSD13 is responsible for the steatosis phenotype in the Hsd17b1333A/A mice.