Consistent with recent observations described by Sharifi et al. [15], this is in sharp contrast to what we observed in mouse derived cell lines, where phosphorylation at Y118-p-paxillin was not required for autophagosomal regulation of paxillin and/or its interaction with LC3 in the mouse mammary tumor derived cell line 4T1, or in FAK −/− or SYF −/− mouse embryonic fibroblasts (data not shown), further supporting a tissue-type specific mechanism for this turnover. This evidence concerns the gene PTK2 and breast cancer.